Pathogenesis of chronic urticaria
Summary Chronic urticaria is defined as the presence of urticaria (hives) for at least 6 weeks with the assumption that it occurs daily or close to it. If we eliminate physical urticarias and urticarial vasculitis from consideration, the remainder can be divided into autoimmune chronic urticaria (45...
Saved in:
| Published in | Clinical and experimental allergy Vol. 39; no. 6; pp. 777 - 787 |
|---|---|
| Main Authors | , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford, UK
Blackwell Publishing Ltd
01.06.2009
Blackwell |
| Subjects | |
| Online Access | Get full text |
Cover
Loading…
| Abstract | Summary
Chronic urticaria is defined as the presence of urticaria (hives) for at least 6 weeks with the assumption that it occurs daily or close to it. If we eliminate physical urticarias and urticarial vasculitis from consideration, the remainder can be divided into autoimmune chronic urticaria (45%) and idiopathic chronic urticaria (55%). The autoimmune subgroup is associated with the IgG anti‐IgE receptor α subunit in 35–40% of patients and IgG anti‐IgE in an additional 5–10%. These autoantibodies have been shown to activate blood basophils and cutaneous mast cells in vitro with augmentation of basophil activation by complement and release of C5a, in particular. Binding methods (immunoblot and ELISA) yield positives in many autoimmune diseases as well as occasional normal subjects or patients with other forms of urticaria but most such sera are non‐functional. Activation of basophils or mast cells causing histamine release is quite specific for chronic urticaria and defines the autoimmune subgroup. Although pathogenicity is not formally proven, the antibodies cause wealing upon intradermal injection, and removal of the autoantibody leads to remission. A cellular infiltrate is seen to be characterized by mast cell degranulation and infiltration of CD4+ T lymphocytes, monocytes, neutrophils, eosinophils, and basophils. The intensity of the infiltrate and clinical severity of the disease (including accompanying angio‐oedema) is more severe in the autoimmune subpopulation. This latter group also has a higher evidence of human leucocyte antigen DR alleles associated with autoimmunity and a 25% incidence of antithyroid antibodies with diagnosed hypothyroidism in some. Hypo‐responsiveness of patients' basophils to anti‐IgE and hyperresponsiveness to serum defines another subpopulation (at least 50%) that overlaps the idiopathic and autoimmune subgroups. Hypo‐responsiveness to anti‐IgE has been shown to be associated with elevated levels of cytoplasmic phosphatases that inhibit degranulation. Reversal of the abnormality is seen with disease remission. Further work will be needed to distinguish whether this is a cause or a consequence of persistent urticaria and to further assess the relationship (or lack thereof) of altered responsiveness (decreased or increased) with the presence or absence of activating autoantibodies. |
|---|---|
| AbstractList | Summary
Chronic urticaria is defined as the presence of urticaria (hives) for at least 6 weeks with the assumption that it occurs daily or close to it. If we eliminate physical urticarias and urticarial vasculitis from consideration, the remainder can be divided into autoimmune chronic urticaria (45%) and idiopathic chronic urticaria (55%). The autoimmune subgroup is associated with the IgG anti‐IgE receptor α subunit in 35–40% of patients and IgG anti‐IgE in an additional 5–10%. These autoantibodies have been shown to activate blood basophils and cutaneous mast cells in vitro with augmentation of basophil activation by complement and release of C5a, in particular. Binding methods (immunoblot and ELISA) yield positives in many autoimmune diseases as well as occasional normal subjects or patients with other forms of urticaria but most such sera are non‐functional. Activation of basophils or mast cells causing histamine release is quite specific for chronic urticaria and defines the autoimmune subgroup. Although pathogenicity is not formally proven, the antibodies cause wealing upon intradermal injection, and removal of the autoantibody leads to remission. A cellular infiltrate is seen to be characterized by mast cell degranulation and infiltration of CD4+ T lymphocytes, monocytes, neutrophils, eosinophils, and basophils. The intensity of the infiltrate and clinical severity of the disease (including accompanying angio‐oedema) is more severe in the autoimmune subpopulation. This latter group also has a higher evidence of human leucocyte antigen DR alleles associated with autoimmunity and a 25% incidence of antithyroid antibodies with diagnosed hypothyroidism in some. Hypo‐responsiveness of patients' basophils to anti‐IgE and hyperresponsiveness to serum defines another subpopulation (at least 50%) that overlaps the idiopathic and autoimmune subgroups. Hypo‐responsiveness to anti‐IgE has been shown to be associated with elevated levels of cytoplasmic phosphatases that inhibit degranulation. Reversal of the abnormality is seen with disease remission. Further work will be needed to distinguish whether this is a cause or a consequence of persistent urticaria and to further assess the relationship (or lack thereof) of altered responsiveness (decreased or increased) with the presence or absence of activating autoantibodies. Chronic urticaria is defined as the presence of urticaria (hives) for at least 6 weeks with the assumption that it occurs daily or close to it. If we eliminate physical urticarias and urticarial vasculitis from consideration, the remainder can be divided into autoimmune chronic urticaria (45%) and idiopathic chronic urticaria (55%). The autoimmune subgroup is associated with the IgG anti-IgE receptor alpha subunit in 35-40% of patients and IgG anti-IgE in an additional 5-10%. These autoantibodies have been shown to activate blood basophils and cutaneous mast cells in vitro with augmentation of basophil activation by complement and release of C5a, in particular. Binding methods (immunoblot and ELISA) yield positives in many autoimmune diseases as well as occasional normal subjects or patients with other forms of urticaria but most such sera are non-functional. Activation of basophils or mast cells causing histamine release is quite specific for chronic urticaria and defines the autoimmune subgroup. Although pathogenicity is not formally proven, the antibodies cause wealing upon intradermal injection, and removal of the autoantibody leads to remission. A cellular infiltrate is seen to be characterized by mast cell degranulation and infiltration of CD4+ T lymphocytes, monocytes, neutrophils, eosinophils, and basophils. The intensity of the infiltrate and clinical severity of the disease (including accompanying angio-oedema) is more severe in the autoimmune subpopulation. This latter group also has a higher evidence of human leucocyte antigen DR alleles associated with autoimmunity and a 25% incidence of antithyroid antibodies with diagnosed hypothyroidism in some. Hypo-responsiveness of patients' basophils to anti-IgE and hyperresponsiveness to serum defines another subpopulation (at least 50%) that overlaps the idiopathic and autoimmune subgroups. Hypo-responsiveness to anti-IgE has been shown to be associated with elevated levels of cytoplasmic phosphatases that inhibit degranulation. Reversal of the abnormality is seen with disease remission. Further work will be needed to distinguish whether this is a cause or a consequence of persistent urticaria and to further assess the relationship (or lack thereof) of altered responsiveness (decreased or increased) with the presence or absence of activating autoantibodies. Chronic urticaria is defined as the presence of urticaria (hives) for at least 6 weeks with the assumption that it occurs daily or close to it. If we eliminate physical urticarias and urticarial vasculitis from consideration, the remainder can be divided into autoimmune chronic urticaria (45%) and idiopathic chronic urticaria (55%). The autoimmune subgroup is associated with the IgG anti‐IgE receptor α subunit in 35–40% of patients and IgG anti‐IgE in an additional 5–10%. These autoantibodies have been shown to activate blood basophils and cutaneous mast cells in vitro with augmentation of basophil activation by complement and release of C5a, in particular. Binding methods (immunoblot and ELISA) yield positives in many autoimmune diseases as well as occasional normal subjects or patients with other forms of urticaria but most such sera are non‐functional. Activation of basophils or mast cells causing histamine release is quite specific for chronic urticaria and defines the autoimmune subgroup. Although pathogenicity is not formally proven, the antibodies cause wealing upon intradermal injection, and removal of the autoantibody leads to remission. A cellular infiltrate is seen to be characterized by mast cell degranulation and infiltration of CD4 + T lymphocytes, monocytes, neutrophils, eosinophils, and basophils. The intensity of the infiltrate and clinical severity of the disease (including accompanying angio‐oedema) is more severe in the autoimmune subpopulation. This latter group also has a higher evidence of human leucocyte antigen DR alleles associated with autoimmunity and a 25% incidence of antithyroid antibodies with diagnosed hypothyroidism in some. Hypo‐responsiveness of patients' basophils to anti‐IgE and hyperresponsiveness to serum defines another subpopulation (at least 50%) that overlaps the idiopathic and autoimmune subgroups. Hypo‐responsiveness to anti‐IgE has been shown to be associated with elevated levels of cytoplasmic phosphatases that inhibit degranulation. Reversal of the abnormality is seen with disease remission. Further work will be needed to distinguish whether this is a cause or a consequence of persistent urticaria and to further assess the relationship (or lack thereof) of altered responsiveness (decreased or increased) with the presence or absence of activating autoantibodies. SummaryChronic urticaria is defined as the presence of urticaria (hives) for at least 6 weeks with the assumption that it occurs daily or close to it. If we eliminate physical urticarias and urticarial vasculitis from consideration, the remainder can be divided into autoimmune chronic urticaria (45%) and idiopathic chronic urticaria (55%). The autoimmune subgroup is associated with the IgG anti-IgE receptor alpha subunit in 35-40% of patients and IgG anti-IgE in an additional 5-10%. These autoantibodies have been shown to activate blood basophils and cutaneous mast cells in vitro with augmentation of basophil activation by complement and release of C5a, in particular. Binding methods (immunoblot and ELISA) yield positives in many autoimmune diseases as well as occasional normal subjects or patients with other forms of urticaria but most such sera are non-functional. Activation of basophils or mast cells causing histamine release is quite specific for chronic urticaria and defines the autoimmune subgroup. Although pathogenicity is not formally proven, the antibodies cause wealing upon intradermal injection, and removal of the autoantibody leads to remission. A cellular infiltrate is seen to be characterized by mast cell degranulation and infiltration of CD4+ T lymphocytes, monocytes, neutrophils, eosinophils, and basophils. The intensity of the infiltrate and clinical severity of the disease (including accompanying angio-oedema) is more severe in the autoimmune subpopulation. This latter group also has a higher evidence of human leucocyte antigen DR alleles associated with autoimmunity and a 25% incidence of antithyroid antibodies with diagnosed hypothyroidism in some. Hypo-responsiveness of patients' basophils to anti-IgE and hyperresponsiveness to serum defines another subpopulation (at least 50%) that overlaps the idiopathic and autoimmune subgroups. Hypo-responsiveness to anti-IgE has been shown to be associated with elevated levels of cytoplasmic phosphatases that inhibit degranulation. Reversal of the abnormality is seen with disease remission. Further work will be needed to distinguish whether this is a cause or a consequence of persistent urticaria and to further assess the relationship (or lack thereof) of altered responsiveness (decreased or increased) with the presence or absence of activating autoantibodies. Chronic urticaria is defined as the presence of urticaria (hives) for at least 6 weeks with the assumption that it occurs daily or close to it. If we eliminate physical urticarias and urticarial vasculitis from consideration, the remainder can be divided into autoimmune chronic urticaria (45%) and idiopathic chronic urticaria (55%). The autoimmune subgroup is associated with the IgG anti-IgE receptor alpha subunit in 35-40% of patients and IgG anti-IgE in an additional 5-10%. These autoantibodies have been shown to activate blood basophils and cutaneous mast cells in vitro with augmentation of basophil activation by complement and release of C5a, in particular. Binding methods (immunoblot and ELISA) yield positives in many autoimmune diseases as well as occasional normal subjects or patients with other forms of urticaria but most such sera are non-functional. Activation of basophils or mast cells causing histamine release is quite specific for chronic urticaria and defines the autoimmune subgroup. Although pathogenicity is not formally proven, the antibodies cause wealing upon intradermal injection, and removal of the autoantibody leads to remission. A cellular infiltrate is seen to be characterized by mast cell degranulation and infiltration of CD4+ T lymphocytes, monocytes, neutrophils, eosinophils, and basophils. The intensity of the infiltrate and clinical severity of the disease (including accompanying angio-oedema) is more severe in the autoimmune subpopulation. This latter group also has a higher evidence of human leucocyte antigen DR alleles associated with autoimmunity and a 25% incidence of antithyroid antibodies with diagnosed hypothyroidism in some. Hypo-responsiveness of patients' basophils to anti-IgE and hyperresponsiveness to serum defines another subpopulation (at least 50%) that overlaps the idiopathic and autoimmune subgroups. Hypo-responsiveness to anti-IgE has been shown to be associated with elevated levels of cytoplasmic phosphatases that inhibit degranulation. Reversal of the abnormality is seen with disease remission. Further work will be needed to distinguish whether this is a cause or a consequence of persistent urticaria and to further assess the relationship (or lack thereof) of altered responsiveness (decreased or increased) with the presence or absence of activating autoantibodies.Chronic urticaria is defined as the presence of urticaria (hives) for at least 6 weeks with the assumption that it occurs daily or close to it. If we eliminate physical urticarias and urticarial vasculitis from consideration, the remainder can be divided into autoimmune chronic urticaria (45%) and idiopathic chronic urticaria (55%). The autoimmune subgroup is associated with the IgG anti-IgE receptor alpha subunit in 35-40% of patients and IgG anti-IgE in an additional 5-10%. These autoantibodies have been shown to activate blood basophils and cutaneous mast cells in vitro with augmentation of basophil activation by complement and release of C5a, in particular. Binding methods (immunoblot and ELISA) yield positives in many autoimmune diseases as well as occasional normal subjects or patients with other forms of urticaria but most such sera are non-functional. Activation of basophils or mast cells causing histamine release is quite specific for chronic urticaria and defines the autoimmune subgroup. Although pathogenicity is not formally proven, the antibodies cause wealing upon intradermal injection, and removal of the autoantibody leads to remission. A cellular infiltrate is seen to be characterized by mast cell degranulation and infiltration of CD4+ T lymphocytes, monocytes, neutrophils, eosinophils, and basophils. The intensity of the infiltrate and clinical severity of the disease (including accompanying angio-oedema) is more severe in the autoimmune subpopulation. This latter group also has a higher evidence of human leucocyte antigen DR alleles associated with autoimmunity and a 25% incidence of antithyroid antibodies with diagnosed hypothyroidism in some. Hypo-responsiveness of patients' basophils to anti-IgE and hyperresponsiveness to serum defines another subpopulation (at least 50%) that overlaps the idiopathic and autoimmune subgroups. Hypo-responsiveness to anti-IgE has been shown to be associated with elevated levels of cytoplasmic phosphatases that inhibit degranulation. Reversal of the abnormality is seen with disease remission. Further work will be needed to distinguish whether this is a cause or a consequence of persistent urticaria and to further assess the relationship (or lack thereof) of altered responsiveness (decreased or increased) with the presence or absence of activating autoantibodies. |
| Author | Kaplan, A. P. Greaves, M. |
| Author_xml | – sequence: 1 givenname: A. P. surname: Kaplan fullname: Kaplan, A. P. organization: Department of Medicine, Division of Pulmonary and Critical Care Medicine, Allergy and Clinical Immunology, Medical University of South Carolina, Charleston, SC, USA and – sequence: 2 givenname: M. surname: Greaves fullname: Greaves, M. organization: The Skin Allergy Clinic, St Johns Institute of Dermatology, St Thomas' Hospital, London, UK |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21440723$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/19400905$$D View this record in MEDLINE/PubMed |
| BookMark | eNqNkUtPGzEQgC0EIiHwF6r0UG67-LlrH1oJUl5S1KIWFG4jr-NtnG52wd6oyb_HS9IceknnYkvzfTP2zAk6rJvaIjQkOCUxLuYpYZlIaIyUYqxSzKjI0tUB6u8Sh6iPleBJLhXvoZMQ5hhjJpQ8Rj2ieLSw6KOPD7qdNb9sbYMLw6YcmplvameGS986o73Tp-io1FWwZ9tzgJ5urh9Hd8n4--396HKcGMFolhSal0oYK2luFSMZJgUpCikZ1bScTmWuC0wyLgUzgnKuFM0pjRydZqWMeTZA55u6L755XdrQwsIFY6tK17ZZBshylhOK2V6QYiF5xkkEP2zBZbGwU3jxbqH9Gv7-PgKftoAORlel17VxYcdRwjnOadfxy4YzvgnB2xKMa3Xrmrr12lVAMHRrgTl004du-tCtBd7XAqtYQP5TYPeW_ernjfrHVXb93x6Mri-7W_STje9Ca1c7X_vf7xMVMPl2CyP-9ep58uMnjNkb6JGvmA |
| CitedBy_id | crossref_primary_10_2196_34586 crossref_primary_10_4103_ETMJ_ETMJ_D_24_00028 crossref_primary_10_1111_j_1468_3083_2011_04185_x crossref_primary_10_25208_0042_4609_2014_90_3_116_120 crossref_primary_10_1111_ddg_14485_g crossref_primary_10_3109_08820139_2014_892509 crossref_primary_10_37545_haematoljbd2023101 crossref_primary_10_1111_j_1398_9995_2010_02506_x crossref_primary_10_1590_S0365_05962012000400010 crossref_primary_10_1080_1744666X_2017_1249467 crossref_primary_10_4161_derm_29727 crossref_primary_10_1371_journal_pone_0109565 crossref_primary_10_1016_j_aller_2013_05_006 crossref_primary_10_1007_s13671_017_0198_1 crossref_primary_10_1007_s13671_012_0036_4 crossref_primary_10_1111_j_1365_2133_2010_09884_x crossref_primary_10_36691_RJA1439 crossref_primary_10_1111_j_1398_9995_2011_02704_x crossref_primary_10_1016_j_jaci_2011_06_010 crossref_primary_10_3928_19382359_20210422_02 crossref_primary_10_1016_j_aller_2015_10_004 crossref_primary_10_1111_1346_8138_14075 crossref_primary_10_1111_j_1399_3038_2010_01120_x crossref_primary_10_1007_s40265_020_01387_9 crossref_primary_10_1007_s11882_012_0268_1 crossref_primary_10_1007_s15007_016_1240_5 crossref_primary_10_25259_IJSA_14_2023 crossref_primary_10_1586_1744666X_2014_892416 crossref_primary_10_1016_j_anai_2016_06_024 crossref_primary_10_4168_aard_2015_3_1_3 crossref_primary_10_1016_j_aller_2014_04_002 crossref_primary_10_1016_j_aller_2014_04_001 crossref_primary_10_1016_j_anai_2016_09_436 crossref_primary_10_1309_AJCPLSN0RQKHJX1A crossref_primary_10_5021_ad_2014_26_2_145 crossref_primary_10_1016_j_jaci_2017_07_026 crossref_primary_10_1080_09546634_2016_1249819 crossref_primary_10_2174_2772270816666220314154951 crossref_primary_10_1016_j_iac_2020_06_005 crossref_primary_10_1371_journal_pone_0150304 crossref_primary_10_4103_ijmr_IJMR_1060_17 crossref_primary_10_4103_jdds_jdds_72_21 crossref_primary_10_1111_j_1365_2222_2011_03878_x crossref_primary_10_1111_jdv_13198 crossref_primary_10_1111_1346_8138_12578 crossref_primary_10_1111_jdv_13196 crossref_primary_10_1016_j_anai_2010_05_003 crossref_primary_10_1016_j_jssdds_2011_04_007 crossref_primary_10_1111_j_1365_2249_2011_04473_x crossref_primary_10_1007_s10753_010_9242_z crossref_primary_10_3390_ijms23179631 crossref_primary_10_1016_j_jaci_2014_05_004 crossref_primary_10_3390_cells10071759 crossref_primary_10_1111_jdv_14548 crossref_primary_10_4168_aair_2017_9_6_477 crossref_primary_10_1007_s11154_018_9450_7 crossref_primary_10_4103_ijdd_ijdd_2_18 crossref_primary_10_2147_JAA_S325657 crossref_primary_10_1111_j_1365_2133_2010_10198_x crossref_primary_10_1016_j_jaip_2019_01_026 crossref_primary_10_1016_j_clim_2017_11_004 crossref_primary_10_1016_j_iac_2013_09_012 crossref_primary_10_1111_j_1365_2249_2011_04485_x crossref_primary_10_1016_j_reval_2010_04_004 crossref_primary_10_3390_jpm13030422 crossref_primary_10_1016_j_clindermatol_2021_12_010 crossref_primary_10_1111_j_1468_3083_2011_04302_x crossref_primary_10_1155_2017_4123694 crossref_primary_10_1016_j_iac_2017_03_001 crossref_primary_10_1111_jdv_13695 crossref_primary_10_1111_ced_13368 crossref_primary_10_1089_thy_2010_0103 crossref_primary_10_3109_09546634_2011_593485 crossref_primary_10_1080_09546634_2018_1543844 crossref_primary_10_1371_journal_pone_0064142 crossref_primary_10_1111_imr_12638 crossref_primary_10_1016_S1761_2896_20_44051_8 crossref_primary_10_1111_j_1399_3038_2011_01225_x crossref_primary_10_1016_j_jaip_2020_07_058 crossref_primary_10_1016_j_jaad_2015_03_041 crossref_primary_10_1186_s12948_017_0059_2 crossref_primary_10_1016_j_jaci_2018_10_064 crossref_primary_10_1097_ACI_0000000000000538 crossref_primary_10_3109_09546634_2011_565015 crossref_primary_10_1111_imr_12632 crossref_primary_10_1016_j_endonu_2011_04_006 crossref_primary_10_1016_j_anai_2010_06_011 crossref_primary_10_1517_14656566_2013_850490 crossref_primary_10_1016_j_imbio_2014_09_004 crossref_primary_10_1016_j_imlet_2023_11_008 crossref_primary_10_21518_2079_701X_2022_16_6_176_180 crossref_primary_10_1097_01_EWX_0000481697_17654_65 crossref_primary_10_1155_2016_5032051 crossref_primary_10_1080_09546634_2018_1551608 crossref_primary_10_1016_j_indmarman_2015_01_012 crossref_primary_10_1016_j_arcmed_2012_10_007 crossref_primary_10_1111_exd_13705 crossref_primary_10_3109_07435800_2012_714432 crossref_primary_10_1016_j_jaad_2009_11_686 crossref_primary_10_1111_j_1365_3164_2012_01117_x crossref_primary_10_33590_emj_19_00162 crossref_primary_10_1016_j_jaad_2009_11_687 crossref_primary_10_1097_ACI_0b013e32833f1ba6 crossref_primary_10_1155_2022_7468453 crossref_primary_10_1007_s12016_012_8326_y crossref_primary_10_3390_cells8020112 crossref_primary_10_1007_s10803_010_1171_z crossref_primary_10_1016_j_intimp_2018_11_025 crossref_primary_10_1155_2016_8163803 crossref_primary_10_4168_aair_2019_11_1_1 crossref_primary_10_1002_msj_20288 crossref_primary_10_3389_fimmu_2014_00231 crossref_primary_10_1016_j_piel_2020_05_007 crossref_primary_10_1007_s00403_011_1144_x crossref_primary_10_1186_s12948_020_00123_8 crossref_primary_10_55544_sjmars_3_5_10 crossref_primary_10_61186_sjku_29_4_39 crossref_primary_10_1111_bph_13784 crossref_primary_10_3389_fendo_2023_1167890 crossref_primary_10_7759_cureus_35809 crossref_primary_10_1586_edm_09_54 crossref_primary_10_3390_ijms241210320 crossref_primary_10_1016_j_jaci_2016_04_051 crossref_primary_10_1002_cia2_12043 crossref_primary_10_1080_09546634_2020_1762838 crossref_primary_10_1038_jid_2015_13 crossref_primary_10_1155_2014_674709 crossref_primary_10_1016_j_hest_2023_08_003 crossref_primary_10_7759_cureus_42287 crossref_primary_10_1111_j_1468_3083_2010_03817_x crossref_primary_10_1016_j_nurpra_2015_05_010 crossref_primary_10_1007_s12414_017_0241_y crossref_primary_10_1016_j_annder_2011_01_023 crossref_primary_10_1016_j_reval_2012_02_154 crossref_primary_10_1016_j_endoen_2011_04_003 crossref_primary_10_1016_j_jaci_2011_08_023 crossref_primary_10_1097_TME_0000000000000097 crossref_primary_10_1016_j_cellimm_2020_104215 crossref_primary_10_1007_s00403_014_1525_z crossref_primary_10_1080_1744666X_2021_1882304 crossref_primary_10_36691_RJA285 crossref_primary_10_1111_srt_13749 crossref_primary_10_1111_ddg_14485 crossref_primary_10_1080_19932820_2024_2420483 crossref_primary_10_1111_j_1365_2230_2010_03914_x crossref_primary_10_3390_ijerph17010176 crossref_primary_10_1111_jdv_13966 crossref_primary_10_1016_j_aller_2013_06_004 crossref_primary_10_1097_CM9_0000000000002172 crossref_primary_10_1016_j_jaci_2016_06_049 crossref_primary_10_1080_00365513_2022_2129436 crossref_primary_10_1016_j_autrev_2011_08_005 crossref_primary_10_1186_s13601_015_0074_7 crossref_primary_10_1002_14651858_CD008596_pub2 crossref_primary_10_1111_all_13083 crossref_primary_10_1016_j_jaip_2020_11_043 crossref_primary_10_33590_emj_10314947 crossref_primary_10_1016_j_jid_2019_06_153 crossref_primary_10_1016_j_alit_2017_09_003 crossref_primary_10_1016_j_vaccine_2009_08_076 crossref_primary_10_5021_ad_2016_28_2_199 crossref_primary_10_29262_ram_v69iSupl1_1037 crossref_primary_10_1016_j_cyto_2011_08_040 crossref_primary_10_1016_j_iac_2024_03_002 crossref_primary_10_1097_MD_0000000000016127 crossref_primary_10_1016_j_jaad_2010_11_030 crossref_primary_10_4168_aair_2012_4_6_326 crossref_primary_10_1016_j_jaad_2018_01_020 crossref_primary_10_1016_j_anai_2014_02_014 crossref_primary_10_5021_ad_2015_27_4_423 crossref_primary_10_1080_09546634_2018_1468062 crossref_primary_10_1177_2150129713511461 crossref_primary_10_1016_j_reval_2010_02_029 crossref_primary_10_1016_j_iac_2016_08_004 crossref_primary_10_2491_jjsth_31_295 crossref_primary_10_1016_S0151_9638_14_70162_0 crossref_primary_10_1016_j_jaci_2011_07_021 crossref_primary_10_1002_clt2_12011 crossref_primary_10_1111_1346_8138_15516 crossref_primary_10_1016_j_jaci_2009_09_055 crossref_primary_10_1002_mus_24635 crossref_primary_10_1080_15569527_2019_1701486 crossref_primary_10_1007_s40521_024_00372_x crossref_primary_10_1155_2016_1381760 crossref_primary_10_1111_ijd_13487 crossref_primary_10_1111_j_1365_2222_2010_03489_x crossref_primary_10_1186_s12906_018_2305_7 crossref_primary_10_36691_RJA299 crossref_primary_10_1016_j_iac_2016_08_011 crossref_primary_10_3904_kjim_2014_29_6_800 crossref_primary_10_4103_jewd_jewd_59_21 crossref_primary_10_36691_RJA1379 crossref_primary_10_1111_j_1468_3083_2012_04573_x crossref_primary_10_1111_j_1365_2222_2010_03625_x crossref_primary_10_1016_j_dsi_2012_06_001 crossref_primary_10_1111_j_1365_2133_2011_10582_x |
| Cites_doi | 10.1159/000235301 10.1046/j.1365-2133.2000.03664.x 10.1111/j.1398-9995.2007.01514.x 10.1067/mai.2001.115484 10.4049/jimmunol.179.2.1353 10.1016/j.jaci.2008.10.050 10.1172/JCI108405 10.1084/jem.183.3.821 10.1159/000066772 10.1016/j.jaad.2006.07.023 10.1016/S1081-1206(10)60644-8 10.1111/1523-1747.ep12538380 10.1016/S0091-6749(98)70283-0 10.1111/j.1365-2133.2005.06646.x 10.1002/(SICI)1521-4141(199904)29:04<1139::AID-IMMU1139>3.0.CO;2-J 10.1067/mai.2002.126782 10.1016/0091-6749(83)90042-8 10.1111/j.1365-2133.2008.08499.x 10.1016/S0091-6749(99)70129-6 10.1016/j.jaci.2006.08.043 10.1016/S1081-1206(10)60069-5 10.1056/NEJM199506293322608 10.1111/j.1365-2222.2005.02380.x 10.1001/archderm.134.1.41 10.1001/archderm.1983.01650320010007 10.1056/NEJM199306033282204 10.1016/0167-5699(93)90244-F 10.1111/j.1365-2133.1986.tb04065.x 10.1111/1523-1747.ep12338544 10.1016/0091-6749(78)90113-6 10.1038/jid.2008.55 10.1034/j.1398-9995.2003.00195.x 10.1067/mai.2002.120954 10.1034/j.1398-9995.2001.00296.x 10.1111/1523-1747.ep12277582 10.1016/j.jaci.2005.12.1343 10.2340/0001555575484487 10.1046/j.1365-2133.2001.04175.x 10.1016/S1382-6689(97)10050-3 10.4049/jimmunol.155.6.3152 10.1016/S0091-6749(95)70055-2 10.1007/978-3-642-85267-1_2 10.1201/b13958-15 10.1016/0140-6736(92)90666-Q 10.1067/mai.2003.1605 10.1111/j.1365-2222.2006.02494.x 10.1027/0838-1925.13.1.23 10.1159/000023902 10.1111/j.1365-2133.1975.tb06732.x 10.1046/j.1523-1747.2002.01733.x 10.1111/j.1365-2222.1991.tb03198.x 10.1016/S0140-6736(86)90423-X 10.1172/JCI511 10.1046/j.1365-2133.1999.02815.x 10.1007/3-211-27377-8_15 10.1016/0091-6749(83)90096-9 10.1111/j.1365-2222.2005.02212.x 10.1111/j.1365-2133.1973.tb08014.x 10.1016/j.jaci.2006.09.035 10.1126/science.7542803 10.1016/S0091-6749(97)70071-X 10.4049/jimmunol.133.6.3282 10.1067/mai.2002.121309 10.1111/1523-1747.ep12462239 10.1111/j.1365-2222.1974.tb01384.x 10.1111/j.1398-9995.1962.tb02937.x |
| ContentType | Journal Article |
| Copyright | 2009 Blackwell Publishing Ltd 2009 INIST-CNRS |
| Copyright_xml | – notice: 2009 Blackwell Publishing Ltd – notice: 2009 INIST-CNRS |
| DBID | BSCLL AAYXX CITATION IQODW CGR CUY CVF ECM EIF NPM 7T5 H94 7X8 |
| DOI | 10.1111/j.1365-2222.2009.03256.x |
| DatabaseName | Istex CrossRef Pascal-Francis Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed Immunology Abstracts AIDS and Cancer Research Abstracts MEDLINE - Academic |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) AIDS and Cancer Research Abstracts Immunology Abstracts MEDLINE - Academic |
| DatabaseTitleList | MEDLINE CrossRef AIDS and Cancer Research Abstracts MEDLINE - Academic |
| Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Medicine Biology |
| EISSN | 1365-2222 |
| EndPage | 787 |
| ExternalDocumentID | 19400905 21440723 10_1111_j_1365_2222_2009_03256_x CEA3256 ark_67375_WNG_C4DBXWRS_L |
| Genre | reviewArticle Journal Article Review |
| GroupedDBID | --- .3N .55 .GA .Y3 05W 0R~ 10A 1OB 1OC 29B 31~ 33P 36B 3O- 3SF 4.4 4P2 50Y 50Z 51W 51X 52M 52N 52O 52P 52R 52S 52T 52U 52V 52W 52X 53G 5GY 5HH 5LA 5RE 5VS 66C 6J9 702 7PT 8-0 8-1 8-3 8-4 8-5 8UM 930 A01 A03 A8Z AAESR AAEVG AAHHS AAKAS AANLZ AAONW AASGY AAXRX AAZKR ABCQN ABCUV ABDBF ABEML ABJNI ABPVW ABQWH ABXGK ACAHQ ACBWZ ACCFJ ACCZN ACGFS ACGOF ACMXC ACPOU ACPRK ACSCC ACXBN ACXQS ADBBV ADBTR ADEOM ADIZJ ADKYN ADMGS ADOZA ADXAS ADZCM ADZMN ADZOD AEEZP AEGXH AEIGN AEIMD AENEX AEQDE AEUQT AEUYR AFBPY AFEBI AFFPM AFGKR AFPWT AFRAH AFZJQ AHBTC AHEFC AHMBA AIACR AITYG AIURR AIWBW AJBDE ALAGY ALMA_UNASSIGNED_HOLDINGS ALUQN AMBMR AMYDB AOETA ASPBG ATUGU AVWKF AZBYB AZFZN AZVAB BAFTC BDRZF BFHJK BHBCM BMXJE BROTX BRXPI BSCLL BY8 C45 CAG COF CS3 D-6 D-7 D-E D-F DCZOG DPXWK DR2 DRFUL DRMAN DRSTM DU5 EAD EAP EAS EBB EBC EBD EBS EBX EDH EJD EMB EMK EMOBN ESTFP ESX EX3 F00 F01 F04 F5P FEDTE FUBAC FZ0 G-S G.N GODZA H.X HF~ HGLYW HVGLF HZI HZ~ IHE IX1 J0M K48 KBYEO LATKE LC2 LC3 LEEKS LH4 LITHE LOXES LP6 LP7 LUTES LW6 LYRES MEWTI MK4 MRFUL MRMAN MRSTM MSFUL MSMAN MSSTM MXFUL MXMAN MXSTM N04 N05 N9A NF~ O66 O9- OIG OVD P2P P2W P2X P2Z P4B P4D PALCI PQQKQ Q.N Q11 QB0 Q~Q R.K RIWAO RJQFR ROL RX1 SAMSI SUPJJ SV3 TEORI TUS UB1 V8K V9Y W8V W99 WBKPD WHWMO WIH WIJ WIK WOHZO WOW WQJ WRC WUP WVDHM WXI WXSBR X7M XG1 YFH YUY ZGI ZXP ZZTAW ~IA ~WT AAHQN AAIPD AAMNL AANHP AAYCA ACRPL ACUHS ACYXJ ADNMO AFWVQ ALVPJ AAYXX AEYWJ AGHNM AGQPQ AGYGG CITATION AAMMB AEFGJ AGXDD AIDQK AIDYY IQODW CGR CUY CVF ECM EIF NPM 7T5 H94 7X8 |
| ID | FETCH-LOGICAL-c5326-ba4f95ce827e931601b1bb8832a2fdd87ab0164853c52449927223162d6f8dd83 |
| IEDL.DBID | DR2 |
| ISSN | 0954-7894 1365-2222 |
| IngestDate | Fri Jul 11 10:41:03 EDT 2025 Fri Jul 11 08:29:57 EDT 2025 Mon Jul 21 05:56:06 EDT 2025 Mon Jul 21 09:13:56 EDT 2025 Thu Apr 24 23:02:11 EDT 2025 Tue Jul 01 02:53:18 EDT 2025 Wed Jan 22 16:29:36 EST 2025 Wed Oct 30 09:49:18 EDT 2024 |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 6 |
| Keywords | Skin disease Chronic Immunology Pathogenesis Urticaria |
| Language | English |
| License | http://onlinelibrary.wiley.com/termsAndConditions#vor CC BY 4.0 |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c5326-ba4f95ce827e931601b1bb8832a2fdd87ab0164853c52449927223162d6f8dd83 |
| Notes | istex:88F14E1515713200C653DCA8C5EFB02642CEF836 ark:/67375/WNG-C4DBXWRS-L ArticleID:CEA3256 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 ObjectType-Review-3 |
| PMID | 19400905 |
| PQID | 20584641 |
| PQPubID | 23462 |
| PageCount | 11 |
| ParticipantIDs | proquest_miscellaneous_67371203 proquest_miscellaneous_20584641 pubmed_primary_19400905 pascalfrancis_primary_21440723 crossref_citationtrail_10_1111_j_1365_2222_2009_03256_x crossref_primary_10_1111_j_1365_2222_2009_03256_x wiley_primary_10_1111_j_1365_2222_2009_03256_x_CEA3256 istex_primary_ark_67375_WNG_C4DBXWRS_L |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | June 2009 |
| PublicationDateYYYYMMDD | 2009-06-01 |
| PublicationDate_xml | – month: 06 year: 2009 text: June 2009 |
| PublicationDecade | 2000 |
| PublicationPlace | Oxford, UK |
| PublicationPlace_xml | – name: Oxford, UK – name: Oxford – name: England |
| PublicationTitle | Clinical and experimental allergy |
| PublicationTitleAlternate | Clin Exp Allergy |
| PublicationYear | 2009 |
| Publisher | Blackwell Publishing Ltd Blackwell |
| Publisher_xml | – name: Blackwell Publishing Ltd – name: Blackwell |
| References | Lee K, Kim J, Kang D, Choi Y, Lee W, Ro J. Increased expression of endothelial cell adhesion molecules due to mediator release from human foreskin mast cells stimulated by autoantibodies in chronic urticaria sera. J Invest Dermatol 2002; 118:658-63. Kaplan A, Joseph K. Basophil secretion in chronic urticaria: autoantibody-dependent or not? J Allergy Clin Immunol 2007; 120:729-30. Ferrer M, Luquin E, Kaplan A. IL3 effect on basophils histamine release upon stimulation with chronic urticaria sera. Allergy 2003; 58:802-7. Young E. Prevelence of intolerance to food additives. Environ Toxicol Pharmacol 1997; 4:111-4. Grattan C, Powell S, Humphreys F. Management and diagnostic guidelines for urticaria and angio-oedema. Br J Dermatol 2001; 144:708-14. Grattan C, Francis D, Slater N, Barlow R, Greaves M. Plasmapheresis for severe, unremitting, chronic urticaria. Lancet 1992; 339:1078-80. Kaplan A. Urticaria and angioedema, 7th Edn. New York: McGraw Hill Publishing, 2007. Kaplan A, Horakova Z, Katz S. Assessment of tissue fluid histamine levels in patients with urticaria. J Allergy Clin Immunol 1978; 61:350-4. Kikuchi Y, Fann T, Kaplan A. Antithyroid antibodies in chronic urticaria and angioedema. J Allergy Clin Immunol 2003; 112:218. Michaelsson G, Juhlin L. Urticaria induced by preservatives and dye additives in food and drugs. Brit J Dermatol 1973; 88:525-32. Grattan C, Wallington T, Warin R, Kennedy C, Bradfield J. A serological mediator in chronic idiopathic urticaria - a clinical, immunological and histological evaluation. Br J Dermatol 1986; 114:583-90. Fiebiger E, Maurer D, Holub H et al. Serum IgG autoantibodies directed against the alpha chain of Fc epsilon RI: a selective marker and pathogenetic factor for a distinct subset of chronic urticaria patients? J Clin Invest 1995; 96:2606-12. Claveau J, Lavoie A, Brunet C, Bedard P, Hebert J. Chronic idiopathic urticaria: possible contribution of histamine-releasing factor to pathogenesis. J Allergy Clin Immunol 1993; 92 (1 Pt 1):132-7. Supramaniam G, Warner J. Artificial food additive intolerance in patients with angio-oedema and urticaria. Lancet 1986; 2:907-9. Fureder W, Agis H, Willheim M et al. Differential expression of complement receptors on human basophils and mast cells. Evidence for mast cell heterogeneity and CD88/C5aR expression on skin mast cells. J Immunol 1995; 155:3152-60. Haas N, Toppe E, Henz B. Microscopic morphology of different types of urticaria. Arch Dermatol 1998; 134:41-6. Kikuchi Y, Kaplan A. A role for C5a in augmenting IgG-dependent histamine release from basophils in chronic urticaria. J Allergy Clin Immunol 2002; 109:114-8. Kikuchi Y, Kaplan A. Mechanisms of autoimmune activation of basophils in chronic urticaria. J Allergy Clin Immunol 2001; 107:1056-62. Puccetti A, Bason C, Simeoni S et al. In chronic idiopathic urticaria autoantibodies against Fc epsilonRII/CD23 induce histamine release via eosinophil activation. Clin Exp Allergy 2005; 35:1599-607. Mathews K. Urticaria and angioedema. J Allergy Clin Immunol 1983; 72:1-14. Sabroe R, Francis D, Barr R, Black A, Greaves M. Anti-Fc(episilon)RI auto antibodies and basophil histamine releasability in chronic idiopathic urticaria. J Allergy Clin Immunol 1998; 102:651-8. O'Donnell B, Francis D, Swana G, Seed P, Kobza Black A, Greaves M. Thyroid autoimmunity in chronic urticaria. Br J Dermatol 2005; 153:331-5. Elias J, Boss E, Kaplan A. Studies of the cellular infiltrate of chronic idiopathic urticaria: prominence of T-lymphocytes, monocytes, and mast cells. J Allergy Clin Immunol 1986; 78:914-8. Spector S, Tan R. Effect of omalizumab on patients with chronic urticaria. Ann Allergy Asthma Immunol 2007; 99:190-3. Grattan C, Boon A, Eady R, Winkelmann R. The pathology of the autologous serum skin test response in chronic urticaria resembles IgE-mediated late-phase reactions. Int Arch Allergy Immunol 1990; 93:198-204. Du Toit G, Prescott R, Lawrence P et al. Autoantibodies to the high-affinity IgE receptor in children with chronic urticaria. J Allergy Clin Immunol 2006; 96:341-4. Razin E, Marx G. Thrombin-induced degranulation of cultured bone marrow-derived mast cells. J Immunol 1984; 133:3282-5. Zuberbier T, Pfrommer C, Specht K et al. Aromatic components of food as novel eliciting factors of pseudoallergic reactions in chronic urticaria. J Allergy Clin Immunol 2002; 109:343-8. Dreyfus D. Observations on the mechanism of omalizumab as a steroid-sparing agent in autoimmune or chronic idiopathic urticaria and angioedema. Ann Allergy Asthma Immunol 2008; 100:624-5. Gomez G, Jogie-Brahim S, Shima M, Schwartz L. Omalizumab reverses the phenotypic and functional effects of IgE-enhanced Fc epsilonRI on human skin mast cells. J Immunol 2007; 179:1353-61. Peters M, Schroeter A, Kephart G, Gleich G. Localization of eosinophil granule major basic protein in chronic urticaria. J Invest Dermatol 1983; 81:39-43. Kern F, Lichtenstein L. Defective histamine release in chronic urticaria. J Clin Invest 1976; 57:1369-77. Kaplan A. Chronic urticaria: pathogenesis and treatment. J Allergy Clin Immunol 2004; 114:465-74. Lourenco F, Azor M, Santos J et al. Activated status of basophils in chronic urticaria leads to interleukin-3 hyper-responsiveness and enhancement of histamine release induced by anti-IgE stimulus. Brit J Dermatol 2008; 158:979-86. Sabroe R, Poon E, Orchard G et al. Cutaneous inflammatory cell infiltrate in chronic idiopathic urticaria: comparison of patients with and without anti-FcepsilonRI or anti-IgE autoantibodies. J Allergy Clin Immunol 1999; 103:484-93. Gruber B, Baeza M, Marchese M, Agnello V, Kaplan AP. Prevalence and functional role of anti-IgE autoantibodies in urticarial syndromes. J Invest Dermatol 1988; 90:213-7. Nettis E, Dambra P, Loria M et al. Mast-cell phenotype in urticaria. Allergy 2001; 56:915-9. Di Lorenzo G, Pacor M, Mansueto P et al. Food-additive-induced urticaria: a survey of 838 patients with recurrent chronic idiopathic urticaria. Int Arch Allergy Immunol 2005; 138:235-42. Hide M, Francis D, Grattan C, Hakimi J, Kochan J, Greaves M. Autoantibodies against the high-affinity IgE receptor as a cause of histamine release in chronic urticaria. N Engl J Med 1993; 328:1599-604. Haas N, Schadendorf D, Henz B. Differential endothelial adhesion molecule expression in early and late whealing reactions. Int Arch Allergy Immunol 1998; 115:210-4. Greaves M. Chronic idiopathic urticaria and Helicobacter pylori- not directly causative but could there be a link. Allergy Clin Immunol Int 2001; 13:23-6. Ferrer M, Luquin E, Sanchez-Ibarrola A, Moreno C, Sanz M, Kaplan A. Secretion of cytokines, histamine and leukotrienes in chronic urticaria. Int Arch Allergy Immunol 2002; 129:254-60. Tong L, Balakrishnan G, Kochan J, Kinet J, Kaplan A. Assessment of autoimmunity in patients with chronic urticaria. J Allergy Clin Immunol 1997; 99:461-5. Niimi N, Francis D, Kermani F et al. Dermal mast cell activation by autoantibodies against the high affinity IgE receptor in chronic urticaria. J Invest Dermatol 1996; 106:1001-6. Marone G, Casolaro V, Paganelli R, Quinti I. IgG anti-IgE from atopic dermatitis induces mediator release from basophils and mast cells. J Invest Dermatol 1989; 93:246-52. Grattan C, Francis D, Hide M, Greaves M. Detection of circulating histamine releasing autoantibodies with functional properties of anti-IgE in chronic urticaria. Clin Exp Allergy 1991; 21:695-704. Asero R, Tedeschi A, Riboldi P, Cugno M. Plasma of patients with chronic urticaria shows signs of thrombin generation, and its intradermal injection causes wheal-and-flare reactions much more frequently than autologous serum. J Allergy Clin Immunol 2006; 117:1113-7. Vonakis B, Vasagar K, Gibbons SJ et al. Basophil FcepsilonRI histamine release parallels expression of Src-homology 2-containing inositol phosphatases in chronic idiopathic urticaria. J Allergy Clin Immunol 2007; 119:441-8. Eckman J, Hamilton R, Gober L, Sterba P, Saini S. Basophil phenotypes in chronic idiopathic urticaria in relation to disease activity and autoantibodies. J Invest Dermatol 2008; 128:1956-63. Leznoff A, Josse R, Denburg J, Dolovich J. Association of chronic urticaria and angioedema with thyroid autoimmunity. Arch Dermatol 1983; 119:636-40. Asero R, Tedeschi A, Riboldi P, Griffini S, Bonanni E, Cugno M. Severe chronic urticaria is associated with elevated plasma levels of D-dimer. Allergy 2007; 63:176-80. Zuberbier T, Bindslev-Jensen C, Canonica W et al. EAACI/GA2LEN/EDF guideline: management of urticaria. Allergy 2006; 61:321-31. O'Donnell B, O'Neill C, Francis D et al. Human leucocyte antigen class II associations in chronic idiopathic urticaria. Br J Dermatol 1999; 140:853-8. Grattan C, Francis D. Autoimmune urticaria. Adv Dermatol 1999; 12:311-40. MacDonald S, Rafnar T, Langdon J, Lichtenstein L. Molecular identification of an IgE-dependent histamine-releasing factor. Science 1995; 269:688-90. Vasagar K, Vonakis B, Gober L, Viksman A, Gibbons SJ, Saini S. Evidence of in vivo basophil activation in chronic idiopathic urticaria. Clin Exp Allergy 2006; 36:770-6. Rose N, Bona C. Defining criteria for autoimmune diseases (Witebsky's postulates revisited). Immunol Today 1993; 14:426-30. Greaves M, Plummer V, McLaughlan P, Stanworth D. Serum and cell bound IgE in chronic urticaria. Clin Allergy 1974; 4:265-71. Luquin E, Kaplan A, Ferrer M. Increased responsiveness of basophils of patients with chronic urticaria to sera but hypo-responsiveness to other stimuli. Clin Exp Allergy 2005; 35:456-60. Rorsman H. Basophilic leucopenia in different forms of urticaria. Acta Allergologica 1962; 17:168-84. Kaplan A, Joseph K, Maykut R, Zeldin R. Treatment of chronic autoimmune urticaria with Omalizumab. J Allergy Clin Immunol 2009; 123:713-7. Asero R, Tedeschi A, Coppola R et al. Activation of the tissue factor pathway of blood coagulation in patients with chronic urticaria. J Allergy Clin Immunol 2007; 119:705-10. Zuberbier T, Chantraine-Hess S, Hartmann K, Czarnetzki B. Pseudoallergen-free diet in the treatment 1989; 84 2001; 144 1995; 75 1993; 328 1986; 78 2005; 138 2006; 36 2003; 58 1996; 183 2002; 118 1999; 163 1998; 115 1995; 332 1975; 93 2001; 107 2008; 100 2003; 112 1997; 4 1996; 106 1983; 119 1974; 4 1986; 2 2007; 179 2006; 61 1997; 99 1973; 88 2005; 145 2002; 40 1978; 61 1999; 12 2009; 123 2008; 158 2002; 109 2007; 63 2001; 56 2001; 13 2005; 35 1990; 93 1995; 96 1986; 114 2006; 96 2005; 153 1999; 29 2006; 16 2007; 120 1998 1962; 17 1999; 140 2007 2008; 128 1999; 4 1983; 71 2005 1999; 103 1983; 72 2004 1995; 155 1998; 139 2002 1988; 90 1999; 104 2007; 99 2006; 117 1998; 134 2007; 56 1993; 14 1989; 93 1976; 57 2007; 119 2004; 114 1991; 21 1993; 92 1984; 133 2002; 129 1995; 269 1992; 339 2000; 143 1983; 81 1998; 102 1998; 101 e_1_2_13_24_2 e_1_2_13_26_2 e_1_2_13_45_2 e_1_2_13_68_2 e_1_2_13_20_2 e_1_2_13_43_2 Grattan C (e_1_2_13_59_2) 1999; 12 e_1_2_13_66_2 e_1_2_13_22_2 e_1_2_13_41_2 Elias J (e_1_2_13_47_2) 1986; 78 e_1_2_13_85_2 e_1_2_13_8_2 e_1_2_13_62_2 e_1_2_13_83_2 e_1_2_13_60_2 e_1_2_13_81_2 Kaplan A. (e_1_2_13_3_2) 2004; 114 Leznoff A (e_1_2_13_18_2) 1989; 84 e_1_2_13_17_2 e_1_2_13_38_2 e_1_2_13_13_2 e_1_2_13_34_2 e_1_2_13_15_2 e_1_2_13_36_2 e_1_2_13_57_2 e_1_2_13_30_2 e_1_2_13_55_2 e_1_2_13_11_2 e_1_2_13_32_2 e_1_2_13_53_2 Greaves M. (e_1_2_13_64_2) 2002 e_1_2_13_51_2 e_1_2_13_72_2 Zuberbier T (e_1_2_13_79_2) 2006; 61 Sabroe R (e_1_2_13_52_2) 1999; 103 Ying S (e_1_2_13_54_2) 1999; 163 Asero R (e_1_2_13_44_2) 2007; 63 Burova G (e_1_2_13_76_2) 1998; 139 Kaplan A. (e_1_2_13_78_2) 2007 e_1_2_13_4_2 e_1_2_13_2_2 Kaplan A (e_1_2_13_58_2) 2007; 120 e_1_2_13_27_2 Claveau J (e_1_2_13_29_2) 1993; 92 Soundararajan S (e_1_2_13_35_2) 2005; 145 e_1_2_13_23_2 e_1_2_13_48_2 e_1_2_13_69_2 e_1_2_13_25_2 e_1_2_13_67_2 e_1_2_13_65_2 e_1_2_13_21_2 e_1_2_13_42_2 e_1_2_13_61_2 Zuberbier T (e_1_2_13_70_2) 1995; 75 e_1_2_13_84_2 Fiebiger E (e_1_2_13_6_2) 1995; 96 e_1_2_13_7_2 e_1_2_13_82_2 e_1_2_13_5_2 e_1_2_13_80_2 e_1_2_13_9_2 e_1_2_13_16_2 e_1_2_13_39_2 Di Lorenzo G (e_1_2_13_74_2) 2005; 138 e_1_2_13_12_2 e_1_2_13_14_2 Kaplan A (e_1_2_13_19_2) 1999; 4 e_1_2_13_37_2 e_1_2_13_56_2 e_1_2_13_31_2 e_1_2_13_77_2 e_1_2_13_10_2 e_1_2_13_33_2 e_1_2_13_75_2 e_1_2_13_50_2 e_1_2_13_73_2 Du Toit G (e_1_2_13_63_2) 2006; 96 e_1_2_13_71_2 Razin E (e_1_2_13_46_2) 1984; 133 Asero R (e_1_2_13_40_2) 2006; 16 e_1_2_13_28_2 e_1_2_13_49_2 |
| References_xml | – reference: Hide M, Francis D, Grattan C, Hakimi J, Kochan J, Greaves M. Autoantibodies against the high-affinity IgE receptor as a cause of histamine release in chronic urticaria. N Engl J Med 1993; 328:1599-604. – reference: Kikuchi Y, Fann T, Kaplan A. Antithyroid antibodies in chronic urticaria and angioedema. J Allergy Clin Immunol 2003; 112:218. – reference: Kikuchi Y, Kaplan A. A role for C5a in augmenting IgG-dependent histamine release from basophils in chronic urticaria. J Allergy Clin Immunol 2002; 109:114-8. – reference: MacDonald S, Rafnar T, Langdon J, Lichtenstein L. Molecular identification of an IgE-dependent histamine-releasing factor. Science 1995; 269:688-90. – reference: Sabroe R, Fiebiger E, Francis D et al. Classification of anti-FcepsilonRI and anti-IgE autoantibodies in chronic idiopathic urticaria and correlation with disease severity. J Allergy Clin Immunol 2002; 40:492-9. – reference: Greaves M. Chronic urticaria. New Engl J Med 1995; 332:1767-72. – reference: Kaplan A. Urticaria and angioedema, 7th Edn. New York: McGraw Hill Publishing, 2007. – reference: Lourenco F, Azor M, Santos J et al. Activated status of basophils in chronic urticaria leads to interleukin-3 hyper-responsiveness and enhancement of histamine release induced by anti-IgE stimulus. Brit J Dermatol 2008; 158:979-86. – reference: Supramaniam G, Warner J. Artificial food additive intolerance in patients with angio-oedema and urticaria. Lancet 1986; 2:907-9. – reference: Zuberbier T, Chantraine-Hess S, Hartmann K, Czarnetzki B. Pseudoallergen-free diet in the treatment of chronic urticaria. A prospective study. Acta Derm Venereol 1995; 75:484-7. – reference: O'Donnell B, O'Neill C, Francis D et al. Human leucocyte antigen class II associations in chronic idiopathic urticaria. Br J Dermatol 1999; 140:853-8. – reference: Grattan C, Powell S, Humphreys F. Management and diagnostic guidelines for urticaria and angio-oedema. Br J Dermatol 2001; 144:708-14. – reference: Grattan C, Francis D, Hide M, Greaves M. Detection of circulating histamine releasing autoantibodies with functional properties of anti-IgE in chronic urticaria. Clin Exp Allergy 1991; 21:695-704. – reference: Kikuchi Y, Kaplan A. Mechanisms of autoimmune activation of basophils in chronic urticaria. J Allergy Clin Immunol 2001; 107:1056-62. – reference: Asero R, Tedeschi A, Coppola R et al. Activation of the tissue factor pathway of blood coagulation in patients with chronic urticaria. J Allergy Clin Immunol 2007; 119:705-10. – reference: Burova G, Mallet A, Greaves M. Is Helicobacter pylori a cause of chronic urticaria. Br J Dermatol 1998; 139 (Suppl. S1):42. – reference: Razin E, Marx G. Thrombin-induced degranulation of cultured bone marrow-derived mast cells. J Immunol 1984; 133:3282-5. – reference: Grattan C, Boon A, Eady R, Winkelmann R. The pathology of the autologous serum skin test response in chronic urticaria resembles IgE-mediated late-phase reactions. Int Arch Allergy Immunol 1990; 93:198-204. – reference: Gruber B, Baeza M, Marchese M, Agnello V, Kaplan AP. Prevalence and functional role of anti-IgE autoantibodies in urticarial syndromes. J Invest Dermatol 1988; 90:213-7. – reference: Smith C, Kepley C, Schwartz L, Lee T. Mast cell number and phenotype in chronic idiopathic urticaria. J Allergy Clin Immunol 1995; 96:360-4. – reference: Horn M, Gerster T, Ochensberger B et al. Human anti-FcepsilonRIalpha autoantibodies isolated from healthy donors cross-react with tetanus toxoid. Eur J Immunol 1999; 29:1139-48. – reference: Kaplan A. Chronic urticaria: pathogenesis and treatment. J Allergy Clin Immunol 2004; 114:465-74. – reference: Di Lorenzo G, Pacor M, Mansueto P et al. Food-additive-induced urticaria: a survey of 838 patients with recurrent chronic idiopathic urticaria. Int Arch Allergy Immunol 2005; 138:235-42. – reference: Spector S, Tan R. Effect of omalizumab on patients with chronic urticaria. Ann Allergy Asthma Immunol 2007; 99:190-3. – reference: Kaplan A, Horakova Z, Katz S. Assessment of tissue fluid histamine levels in patients with urticaria. J Allergy Clin Immunol 1978; 61:350-4. – reference: Asero R, Madonini E. Bronchial hyperresponsiveness is a common feature in patients with chronic urticaria. J Invest Allergol Clin Immunol 2006; 16:19-23. – reference: Du Toit G, Prescott R, Lawrence P et al. Autoantibodies to the high-affinity IgE receptor in children with chronic urticaria. J Allergy Clin Immunol 2006; 96:341-4. – reference: Haas N, Schadendorf D, Henz B. Differential endothelial adhesion molecule expression in early and late whealing reactions. Int Arch Allergy Immunol 1998; 115:210-4. – reference: Tong L, Balakrishnan G, Kochan J, Kinet J, Kaplan A. Assessment of autoimmunity in patients with chronic urticaria. J Allergy Clin Immunol 1997; 99:461-5. – reference: Claveau J, Lavoie A, Brunet C, Bedard P, Hebert J. Chronic idiopathic urticaria: possible contribution of histamine-releasing factor to pathogenesis. J Allergy Clin Immunol 1993; 92 (1 Pt 1):132-7. – reference: Kaplan A, Joseph K, Maykut R, Zeldin R. Treatment of chronic autoimmune urticaria with Omalizumab. J Allergy Clin Immunol 2009; 123:713-7. – reference: Ferrer M, Nakazawa K, Kaplan A. Complement dependence of histamine release in chronic urticaria. J Allergy Clin Immunol 1999; 104:169-72. – reference: Vasagar K, Vonakis B, Gober L, Viksman A, Gibbons SJ, Saini S. Evidence of in vivo basophil activation in chronic idiopathic urticaria. Clin Exp Allergy 2006; 36:770-6. – reference: Dreyfus D. Observations on the mechanism of omalizumab as a steroid-sparing agent in autoimmune or chronic idiopathic urticaria and angioedema. Ann Allergy Asthma Immunol 2008; 100:624-5. – reference: Ying S, Robinson D, Meng Q et al. C-C chemokines in allergen-induced late-phase cutaneous responses in atopic subjects: association of eotaxin with early 6-hour eosinophils, and of eotaxin-2 and monocyte chemoattractant protein-4 with the later 24-hour tissue eosinophilia, and relationship to basophils and other C-C chemokines (monocyte chemoattractant protein-3 and RANTES). J Immunol 1999; 163:3976-84. – reference: Guerra L, Rogkakou A, Massacane P et al. Role of contact sensitization in chronic urticaria. J Am Acad Dermatol 2007; 56:88-90. – reference: Nettis E, Dambra P, Loria M et al. Mast-cell phenotype in urticaria. Allergy 2001; 56:915-9. – reference: Fureder W, Agis H, Willheim M et al. Differential expression of complement receptors on human basophils and mast cells. Evidence for mast cell heterogeneity and CD88/C5aR expression on skin mast cells. J Immunol 1995; 155:3152-60. – reference: Kaplan A, Joseph K. Basophil secretion in chronic urticaria: autoantibody-dependent or not? J Allergy Clin Immunol 2007; 120:729-30. – reference: Puccetti A, Bason C, Simeoni S et al. In chronic idiopathic urticaria autoantibodies against Fc epsilonRII/CD23 induce histamine release via eosinophil activation. Clin Exp Allergy 2005; 35:1599-607. – reference: Leznoff A, Josse R, Denburg J, Dolovich J. Association of chronic urticaria and angioedema with thyroid autoimmunity. Arch Dermatol 1983; 119:636-40. – reference: O'Donnell B, Francis D, Swana G, Seed P, Kobza Black A, Greaves M. Thyroid autoimmunity in chronic urticaria. Br J Dermatol 2005; 153:331-5. – reference: Peters M, Schroeter A, Kephart G, Gleich G. Localization of eosinophil granule major basic protein in chronic urticaria. J Invest Dermatol 1983; 81:39-43. – reference: Asero R, Tedeschi A, Riboldi P, Cugno M. Plasma of patients with chronic urticaria shows signs of thrombin generation, and its intradermal injection causes wheal-and-flare reactions much more frequently than autologous serum. J Allergy Clin Immunol 2006; 117:1113-7. – reference: Doeglas H. Reactions to aspirin and food additives in patients with chronic urticaria, including the physical urticarias. Br J Dermatol 1975; 93:135-44. – reference: Kern F, Lichtenstein L. Defective histamine release in chronic urticaria. J Clin Invest 1976; 57:1369-77. – reference: Haas N, Toppe E, Henz B. Microscopic morphology of different types of urticaria. Arch Dermatol 1998; 134:41-6. – reference: Young E. Prevelence of intolerance to food additives. Environ Toxicol Pharmacol 1997; 4:111-4. – reference: Vonakis B, Vasagar K, Gibbons SJ et al. Basophil FcepsilonRI histamine release parallels expression of Src-homology 2-containing inositol phosphatases in chronic idiopathic urticaria. J Allergy Clin Immunol 2007; 119:441-8. – reference: Sabroe R, Francis D, Barr R, Black A, Greaves M. Anti-Fc(episilon)RI auto antibodies and basophil histamine releasability in chronic idiopathic urticaria. J Allergy Clin Immunol 1998; 102:651-8. – reference: Cirino G, Cicala C, Bucci M, Sorrentino L, Maraganore J, Stone S. Thrombin functions as an inflammatory mediator through activation of its receptor. J Exp Med 1996; 183:821-7. – reference: Fiebiger E, Hammerschmid F, Stingl G, Maurer D. Anti-FcepsilonRIalpha autoantibodies in autoimmune-mediated disorders. Identification of a structure-function relationship. J Clin Invest 1998; 101:243-51. – reference: Lee K, Kim J, Kang D, Choi Y, Lee W, Ro J. Increased expression of endothelial cell adhesion molecules due to mediator release from human foreskin mast cells stimulated by autoantibodies in chronic urticaria sera. J Invest Dermatol 2002; 118:658-63. – reference: Kaplan A, Finn A. Autoimmunity and the etiology of chronic urticaria. Can J Allergy Clin Immunol 1999; 4:286-92. – reference: Zuberbier T, Bindslev-Jensen C, Canonica W et al. EAACI/GA2LEN/EDF guideline: management of urticaria. Allergy 2006; 61:321-31. – reference: Sabroe R, Poon E, Orchard G et al. Cutaneous inflammatory cell infiltrate in chronic idiopathic urticaria: comparison of patients with and without anti-FcepsilonRI or anti-IgE autoantibodies. J Allergy Clin Immunol 1999; 103:484-93. – reference: Grattan C, Wallington T, Warin R, Kennedy C, Bradfield J. A serological mediator in chronic idiopathic urticaria - a clinical, immunological and histological evaluation. Br J Dermatol 1986; 114:583-90. – reference: Rorsman H. Basophilic leucopenia in different forms of urticaria. Acta Allergologica 1962; 17:168-84. – reference: Luquin E, Kaplan A, Ferrer M. Increased responsiveness of basophils of patients with chronic urticaria to sera but hypo-responsiveness to other stimuli. Clin Exp Allergy 2005; 35:456-60. – reference: Asero R, Tedeschi A, Riboldi P, Griffini S, Bonanni E, Cugno M. Severe chronic urticaria is associated with elevated plasma levels of D-dimer. Allergy 2007; 63:176-80. – reference: Grattan C, Francis D, Slater N, Barlow R, Greaves M. Plasmapheresis for severe, unremitting, chronic urticaria. Lancet 1992; 339:1078-80. – reference: Fiebiger E, Maurer D, Holub H et al. Serum IgG autoantibodies directed against the alpha chain of Fc epsilon RI: a selective marker and pathogenetic factor for a distinct subset of chronic urticaria patients? J Clin Invest 1995; 96:2606-12. – reference: Elias J, Boss E, Kaplan A. Studies of the cellular infiltrate of chronic idiopathic urticaria: prominence of T-lymphocytes, monocytes, and mast cells. J Allergy Clin Immunol 1986; 78:914-8. – reference: Marone G, Casolaro V, Paganelli R, Quinti I. IgG anti-IgE from atopic dermatitis induces mediator release from basophils and mast cells. J Invest Dermatol 1989; 93:246-52. – reference: Soundararajan S, Kikuchi Y, Joseph K, Kaplan A. Isolation of the pathogenic IgG subclasses in chronic autoimmune urticaria: evidence that IgG1, IgG3, and IgG4 contain antireceptor antibodies that activate basophils while IgG2 is inactive. J Allergy Clin Immunol 2005; 145:815-21. – reference: Michaelsson G, Juhlin L. Urticaria induced by preservatives and dye additives in food and drugs. Brit J Dermatol 1973; 88:525-32. – reference: Natbony S, Phillips M, Elias J, Godfrey H, Kaplan A. Histologic studies of chronic idiopathic urticaria. J Allergy Clin Immunol 1983; 71:177-83. – reference: Rose N, Bona C. Defining criteria for autoimmune diseases (Witebsky's postulates revisited). Immunol Today 1993; 14:426-30. – reference: Gomez G, Jogie-Brahim S, Shima M, Schwartz L. Omalizumab reverses the phenotypic and functional effects of IgE-enhanced Fc epsilonRI on human skin mast cells. J Immunol 2007; 179:1353-61. – reference: Niimi N, Francis D, Kermani F et al. Dermal mast cell activation by autoantibodies against the high affinity IgE receptor in chronic urticaria. J Invest Dermatol 1996; 106:1001-6. – reference: Greaves M, Plummer V, McLaughlan P, Stanworth D. Serum and cell bound IgE in chronic urticaria. Clin Allergy 1974; 4:265-71. – reference: Ferrer M, Luquin E, Sanchez-Ibarrola A, Moreno C, Sanz M, Kaplan A. Secretion of cytokines, histamine and leukotrienes in chronic urticaria. Int Arch Allergy Immunol 2002; 129:254-60. – reference: Ferrer M, Luquin E, Kaplan A. IL3 effect on basophils histamine release upon stimulation with chronic urticaria sera. Allergy 2003; 58:802-7. – reference: Grattan C, Francis D. Autoimmune urticaria. Adv Dermatol 1999; 12:311-40. – reference: Mathews K. Urticaria and angioedema. J Allergy Clin Immunol 1983; 72:1-14. – reference: Grattan C, O'Donnell B, Francis D et al. Randomized double-blind study of cyclosporin in chronic 'idiopathic' urticaria. Br J Dermatol 2000; 143:365-72. – reference: Greaves M. Chronic idiopathic urticaria and Helicobacter pylori- not directly causative but could there be a link. Allergy Clin Immunol Int 2001; 13:23-6. – reference: Leznoff A, Sussman G. Syndrome of idiopathic chronic urticaria and angioedema with thyroid autoimmunity: a study of 90 patients. J Allergy Clin Immunol 1989; 84:66-71. – reference: Eckman J, Hamilton R, Gober L, Sterba P, Saini S. Basophil phenotypes in chronic idiopathic urticaria in relation to disease activity and autoantibodies. J Invest Dermatol 2008; 128:1956-63. – reference: Zuberbier T, Pfrommer C, Specht K et al. Aromatic components of food as novel eliciting factors of pseudoallergic reactions in chronic urticaria. J Allergy Clin Immunol 2002; 109:343-8. – volume: 112 start-page: 218 year: 2003 article-title: Antithyroid antibodies in chronic urticaria and angioedema publication-title: J Allergy Clin Immunol – volume: 117 start-page: 1113 year: 2006 end-page: 7 article-title: Plasma of patients with chronic urticaria shows signs of thrombin generation, and its intradermal injection causes wheal‐and‐flare reactions much more frequently than autologous serum publication-title: J Allergy Clin Immunol – volume: 109 start-page: 343 year: 2002 end-page: 8 article-title: Aromatic components of food as novel eliciting factors of pseudoallergic reactions in chronic urticaria publication-title: J Allergy Clin Immunol – volume: 106 start-page: 1001 year: 1996 end-page: 6 article-title: Dermal mast cell activation by autoantibodies against the high affinity IgE receptor in chronic urticaria publication-title: J Invest Dermatol – volume: 56 start-page: 915 year: 2001 end-page: 9 article-title: Mast‐cell phenotype in urticaria publication-title: Allergy – volume: 123 start-page: 713 year: 2009 end-page: 7 article-title: Treatment of chronic autoimmune urticaria with Omalizumab publication-title: J Allergy Clin Immunol – volume: 4 start-page: 265 year: 1974 end-page: 71 article-title: Serum and cell bound IgE in chronic urticaria publication-title: Clin Allergy – volume: 2 start-page: 907 year: 1986 end-page: 9 article-title: Artificial food additive intolerance in patients with angio‐oedema and urticaria publication-title: Lancet – volume: 61 start-page: 321 year: 2006 end-page: 31 article-title: EAACI/GA2LEN/EDF guideline publication-title: management of urticaria – volume: 35 start-page: 456 year: 2005 end-page: 60 article-title: Increased responsiveness of basophils of patients with chronic urticaria to sera but hypo‐responsiveness to other stimuli publication-title: Clin Exp Allergy – volume: 14 start-page: 426 year: 1993 end-page: 30 article-title: Defining criteria for autoimmune diseases (Witebsky's postulates revisited) publication-title: Immunol Today – start-page: 309 year: 2005 end-page: 32 – volume: 36 start-page: 770 year: 2006 end-page: 6 article-title: Evidence of in vivo basophil activation in chronic idiopathic urticaria publication-title: Clin Exp Allergy – volume: 61 start-page: 350 year: 1978 end-page: 4 article-title: Assessment of tissue fluid histamine levels in patients with urticaria publication-title: J Allergy Clin Immunol – volume: 12 start-page: 311 year: 1999 end-page: 40 article-title: Autoimmune urticaria publication-title: Adv Dermatol – volume: 183 start-page: 821 year: 1996 end-page: 7 article-title: Thrombin functions as an inflammatory mediator through activation of its receptor publication-title: J Exp Med – volume: 107 start-page: 1056 year: 2001 end-page: 62 article-title: Mechanisms of autoimmune activation of basophils in chronic urticaria publication-title: J Allergy Clin Immunol – volume: 179 start-page: 1353 year: 2007 end-page: 61 article-title: Omalizumab reverses the phenotypic and functional effects of IgE‐enhanced Fc epsilonRI on human skin mast cells publication-title: J Immunol – volume: 115 start-page: 210 year: 1998 end-page: 4 article-title: Differential endothelial adhesion molecule expression in early and late whealing reactions publication-title: Int Arch Allergy Immunol – volume: 155 start-page: 3152 year: 1995 end-page: 60 article-title: Differential expression of complement receptors on human basophils and mast cells. Evidence for mast cell heterogeneity and CD88/C5aR expression on skin mast cells publication-title: J Immunol – volume: 101 start-page: 243 year: 1998 end-page: 51 article-title: Anti‐FcepsilonRIalpha autoantibodies in autoimmune‐mediated disorders. Identification of a structure‐function relationship publication-title: J Clin Invest – volume: 71 start-page: 177 year: 1983 end-page: 83 article-title: Histologic studies of chronic idiopathic urticaria publication-title: J Allergy Clin Immunol – volume: 102 start-page: 651 year: 1998 end-page: 8 article-title: Anti‐Fc(episilon)RI auto antibodies and basophil histamine releasability in chronic idiopathic urticaria publication-title: J Allergy Clin Immunol – volume: 29 start-page: 1139 year: 1999 end-page: 48 article-title: Human anti‐FcepsilonRIalpha autoantibodies isolated from healthy donors cross‐react with tetanus toxoid publication-title: Eur J Immunol – volume: 75 start-page: 484 year: 1995 end-page: 7 article-title: Pseudoallergen‐free diet in the treatment of chronic urticaria. A prospective study publication-title: Acta Derm Venereol – volume: 99 start-page: 190 year: 2007 end-page: 3 article-title: Effect of omalizumab on patients with chronic urticaria publication-title: Ann Allergy Asthma Immunol – volume: 57 start-page: 1369 year: 1976 end-page: 77 article-title: Defective histamine release in chronic urticaria publication-title: J Clin Invest – volume: 158 start-page: 979 year: 2008 end-page: 86 article-title: Activated status of basophils in chronic urticaria leads to interleukin‐3 hyper‐responsiveness and enhancement of histamine release induced by anti‐IgE stimulus publication-title: Brit J Dermatol – volume: 81 start-page: 39 year: 1983 end-page: 43 article-title: Localization of eosinophil granule major basic protein in chronic urticaria publication-title: J Invest Dermatol – start-page: 321 year: 2004 end-page: 41 – volume: 63 start-page: 176 year: 2007 end-page: 80 article-title: Severe chronic urticaria is associated with elevated plasma levels of D‐dimer publication-title: Allergy – volume: 109 start-page: 114 year: 2002 end-page: 8 article-title: A role for C5a in augmenting IgG‐dependent histamine release from basophils in chronic urticaria publication-title: J Allergy Clin Immunol – volume: 93 start-page: 246 year: 1989 end-page: 52 article-title: IgG anti‐IgE from atopic dermatitis induces mediator release from basophils and mast cells publication-title: J Invest Dermatol – volume: 144 start-page: 708 year: 2001 end-page: 14 article-title: Management and diagnostic guidelines for urticaria and angio‐oedema publication-title: Br J Dermatol – volume: 92 start-page: 132 issue: (1 Pt 1) year: 1993 end-page: 7 article-title: Chronic idiopathic urticaria publication-title: possible contribution of histamine-releasing factor to pathogenesis – volume: 4 start-page: 111 year: 1997 end-page: 4 article-title: Prevelence of intolerance to food additives publication-title: Environ Toxicol Pharmacol – volume: 103 start-page: 484 year: 1999 end-page: 93 article-title: Cutaneous inflammatory cell infiltrate in chronic idiopathic urticaria publication-title: comparison of patients with and without anti-FcepsilonRI or anti-IgE autoantibodies – volume: 13 start-page: 23 year: 2001 end-page: 6 article-title: Chronic idiopathic urticaria and – not directly causative but could there be a link publication-title: Allergy Clin Immunol Int – volume: 332 start-page: 1767 year: 1995 end-page: 72 article-title: Chronic urticaria publication-title: New Engl J Med – volume: 93 start-page: 135 year: 1975 end-page: 44 article-title: Reactions to aspirin and food additives in patients with chronic urticaria, including the physical urticarias publication-title: Br J Dermatol – volume: 96 start-page: 341 year: 2006 end-page: 4 article-title: Autoantibodies to the high‐affinity IgE receptor in children with chronic urticaria publication-title: J Allergy Clin Immunol – volume: 96 start-page: 2606 year: 1995 end-page: 12 article-title: Serum IgG autoantibodies directed against the alpha chain of Fc epsilon RI publication-title: a selective marker and pathogenetic factor for a distinct subset of chronic urticaria patients? – volume: 96 start-page: 360 year: 1995 end-page: 4 article-title: Mast cell number and phenotype in chronic idiopathic urticaria publication-title: J Allergy Clin Immunol – volume: 17 start-page: 168 year: 1962 end-page: 84 article-title: Basophilic leucopenia in different forms of urticaria publication-title: Acta Allergologica – volume: 40 start-page: 492 year: 2002 end-page: 9 article-title: Classification of anti‐FcepsilonRI and anti‐IgE autoantibodies in chronic idiopathic urticaria and correlation with disease severity publication-title: J Allergy Clin Immunol – volume: 56 start-page: 88 year: 2007 end-page: 90 article-title: Role of contact sensitization in chronic urticaria publication-title: J Am Acad Dermatol – volume: 139 start-page: 42 issue: (Suppl. S1) year: 1998 article-title: Is a cause of chronic urticaria publication-title: Br J Dermatol – volume: 118 start-page: 658 year: 2002 end-page: 63 article-title: Increased expression of endothelial cell adhesion molecules due to mediator release from human foreskin mast cells stimulated by autoantibodies in chronic urticaria sera publication-title: J Invest Dermatol – volume: 58 start-page: 802 year: 2003 end-page: 7 article-title: IL3 effect on basophils histamine release upon stimulation with chronic urticaria sera publication-title: Allergy – volume: 133 start-page: 3282 year: 1984 end-page: 5 article-title: Thrombin‐induced degranulation of cultured bone marrow‐derived mast cells publication-title: J Immunol – year: 2007 – start-page: 19 year: 1998 end-page: 21 – volume: 269 start-page: 688 year: 1995 end-page: 90 article-title: Molecular identification of an IgE‐dependent histamine‐releasing factor publication-title: Science – volume: 120 start-page: 729 year: 2007 end-page: 30 article-title: Basophil secretion in chronic urticaria publication-title: autoantibody-dependent or not? – volume: 21 start-page: 695 year: 1991 end-page: 704 article-title: Detection of circulating histamine releasing autoantibodies with functional properties of anti‐IgE in chronic urticaria publication-title: Clin Exp Allergy – volume: 143 start-page: 365 year: 2000 end-page: 72 article-title: Randomized double‐blind study of cyclosporin in chronic ‘idiopathic’ urticaria publication-title: Br J Dermatol – volume: 99 start-page: 461 year: 1997 end-page: 5 article-title: Assessment of autoimmunity in patients with chronic urticaria publication-title: J Allergy Clin Immunol – volume: 16 start-page: 19 year: 2006 end-page: 23 article-title: Bronchial hyperresponsiveness is a common feature in patients with chronic urticaria publication-title: J Invest Allergol Clin Immunol – volume: 339 start-page: 1078 year: 1992 end-page: 80 article-title: Plasmapheresis for severe, unremitting, chronic urticaria publication-title: Lancet – volume: 72 start-page: 1 year: 1983 end-page: 14 article-title: Urticaria and angioedema publication-title: J Allergy Clin Immunol – volume: 138 start-page: 235 year: 2005 end-page: 42 article-title: Food‐additive‐induced urticaria publication-title: a survey of 838 patients with recurrent chronic idiopathic urticaria – volume: 78 start-page: 914 year: 1986 end-page: 8 article-title: Studies of the cellular infiltrate of chronic idiopathic urticaria publication-title: prominence of T-lymphocytes, monocytes, and mast cells – volume: 129 start-page: 254 year: 2002 end-page: 60 article-title: Secretion of cytokines, histamine and leukotrienes in chronic urticaria publication-title: Int Arch Allergy Immunol – volume: 328 start-page: 1599 year: 1993 end-page: 604 article-title: Autoantibodies against the high‐affinity IgE receptor as a cause of histamine release in chronic urticaria publication-title: N Engl J Med – volume: 145 start-page: 815 year: 2005 end-page: 21 article-title: Isolation of the pathogenic IgG subclasses in chronic autoimmune urticaria publication-title: evidence that IgG1, IgG3, and IgG4 contain antireceptor antibodies that activate basophils while IgG2 is inactive – volume: 114 start-page: 465 year: 2004 end-page: 74 article-title: Chronic urticaria publication-title: pathogenesis and treatment – volume: 90 start-page: 213 year: 1988 end-page: 7 article-title: Prevalence and functional role of anti‐IgE autoantibodies in urticarial syndromes publication-title: J Invest Dermatol – volume: 114 start-page: 583 year: 1986 end-page: 90 article-title: A serological mediator in chronic idiopathic urticaria – a clinical, immunological and histological evaluation publication-title: Br J Dermatol – volume: 93 start-page: 198 year: 1990 end-page: 204 article-title: The pathology of the autologous serum skin test response in chronic urticaria resembles IgE‐mediated late‐phase reactions publication-title: Int Arch Allergy Immunol – volume: 128 start-page: 1956 year: 2008 end-page: 63 article-title: Basophil phenotypes in chronic idiopathic urticaria in relation to disease activity and autoantibodies publication-title: J Invest Dermatol – volume: 88 start-page: 525 year: 1973 end-page: 32 article-title: Urticaria induced by preservatives and dye additives in food and drugs publication-title: Brit J Dermatol – volume: 84 start-page: 66 year: 1989 end-page: 71 article-title: Syndrome of idiopathic chronic urticaria and angioedema with thyroid autoimmunity publication-title: a study of 90 patients – volume: 100 start-page: 624 year: 2008 end-page: 5 article-title: Observations on the mechanism of omalizumab as a steroid‐sparing agent in autoimmune or chronic idiopathic urticaria and angioedema publication-title: Ann Allergy Asthma Immunol – volume: 4 start-page: 286 year: 1999 end-page: 92 article-title: Autoimmunity and the etiology of chronic urticaria publication-title: Can J Allergy Clin Immunol – volume: 119 start-page: 705 year: 2007 end-page: 10 article-title: Activation of the tissue factor pathway of blood coagulation in patients with chronic urticaria publication-title: J Allergy Clin Immunol – start-page: 623 year: 2002 end-page: 9 – volume: 119 start-page: 441 year: 2007 end-page: 8 article-title: Basophil FcepsilonRI histamine release parallels expression of Src‐homology 2‐containing inositol phosphatases in chronic idiopathic urticaria publication-title: J Allergy Clin Immunol – volume: 119 start-page: 636 year: 1983 end-page: 40 article-title: Association of chronic urticaria and angioedema with thyroid autoimmunity publication-title: Arch Dermatol – volume: 134 start-page: 41 year: 1998 end-page: 6 article-title: Microscopic morphology of different types of urticaria publication-title: Arch Dermatol – volume: 163 start-page: 3976 year: 1999 end-page: 84 article-title: C‐C chemokines in allergen‐induced late‐phase cutaneous responses in atopic subjects publication-title: association of eotaxin with early 6-hour eosinophils, and of eotaxin-2 and monocyte chemoattractant protein-4 with the later 24-hour tissue eosinophilia, and relationship to basophils and other C-C chemokines (monocyte chemoattractant protein-3 and RANTES) – volume: 140 start-page: 853 year: 1999 end-page: 8 article-title: Human leucocyte antigen class II associations in chronic idiopathic urticaria publication-title: Br J Dermatol – volume: 153 start-page: 331 year: 2005 end-page: 5 article-title: Thyroid autoimmunity in chronic urticaria publication-title: Br J Dermatol – volume: 104 start-page: 169 year: 1999 end-page: 72 article-title: Complement dependence of histamine release in chronic urticaria publication-title: J Allergy Clin Immunol – volume: 35 start-page: 1599 year: 2005 end-page: 607 article-title: In chronic idiopathic urticaria autoantibodies against Fc epsilonRII/CD23 induce histamine release via eosinophil activation publication-title: Clin Exp Allergy – volume: 16 start-page: 19 year: 2006 ident: e_1_2_13_40_2 article-title: Bronchial hyperresponsiveness is a common feature in patients with chronic urticaria publication-title: J Invest Allergol Clin Immunol – ident: e_1_2_13_32_2 doi: 10.1159/000235301 – ident: e_1_2_13_81_2 doi: 10.1046/j.1365-2133.2000.03664.x – volume: 63 start-page: 176 year: 2007 ident: e_1_2_13_44_2 article-title: Severe chronic urticaria is associated with elevated plasma levels of D‐dimer publication-title: Allergy doi: 10.1111/j.1398-9995.2007.01514.x – ident: e_1_2_13_8_2 doi: 10.1067/mai.2001.115484 – start-page: 623 volume-title: Food allergy and intolerance year: 2002 ident: e_1_2_13_64_2 – ident: e_1_2_13_85_2 doi: 10.4049/jimmunol.179.2.1353 – ident: e_1_2_13_82_2 doi: 10.1016/j.jaci.2008.10.050 – ident: e_1_2_13_10_2 doi: 10.1172/JCI108405 – ident: e_1_2_13_45_2 doi: 10.1084/jem.183.3.821 – ident: e_1_2_13_57_2 doi: 10.1159/000066772 – ident: e_1_2_13_73_2 doi: 10.1016/j.jaad.2006.07.023 – ident: e_1_2_13_83_2 doi: 10.1016/S1081-1206(10)60644-8 – ident: e_1_2_13_53_2 doi: 10.1111/1523-1747.ep12538380 – ident: e_1_2_13_11_2 doi: 10.1016/S0091-6749(98)70283-0 – ident: e_1_2_13_20_2 doi: 10.1111/j.1365-2133.2005.06646.x – ident: e_1_2_13_36_2 doi: 10.1002/(SICI)1521-4141(199904)29:04<1139::AID-IMMU1139>3.0.CO;2-J – ident: e_1_2_13_33_2 doi: 10.1067/mai.2002.126782 – ident: e_1_2_13_69_2 doi: 10.1016/0091-6749(83)90042-8 – volume: 139 start-page: 42 issue: 1 year: 1998 ident: e_1_2_13_76_2 article-title: Is Helicobacter pylori a cause of chronic urticaria publication-title: Br J Dermatol – ident: e_1_2_13_24_2 doi: 10.1111/j.1365-2133.2008.08499.x – ident: e_1_2_13_37_2 doi: 10.1016/S0091-6749(99)70129-6 – ident: e_1_2_13_43_2 doi: 10.1016/j.jaci.2006.08.043 – volume: 103 start-page: 484 year: 1999 ident: e_1_2_13_52_2 article-title: Cutaneous inflammatory cell infiltrate in chronic idiopathic urticaria publication-title: comparison of patients with and without anti-FcepsilonRI or anti-IgE autoantibodies – ident: e_1_2_13_84_2 doi: 10.1016/S1081-1206(10)60069-5 – ident: e_1_2_13_2_2 doi: 10.1056/NEJM199506293322608 – ident: e_1_2_13_41_2 doi: 10.1111/j.1365-2222.2005.02380.x – ident: e_1_2_13_51_2 doi: 10.1001/archderm.134.1.41 – ident: e_1_2_13_17_2 doi: 10.1001/archderm.1983.01650320010007 – ident: e_1_2_13_4_2 doi: 10.1056/NEJM199306033282204 – ident: e_1_2_13_61_2 doi: 10.1016/0167-5699(93)90244-F – ident: e_1_2_13_30_2 doi: 10.1111/j.1365-2133.1986.tb04065.x – volume-title: Urticaria and angioedema year: 2007 ident: e_1_2_13_78_2 – ident: e_1_2_13_5_2 doi: 10.1111/1523-1747.ep12338544 – ident: e_1_2_13_15_2 doi: 10.1016/0091-6749(78)90113-6 – ident: e_1_2_13_14_2 doi: 10.1038/jid.2008.55 – ident: e_1_2_13_25_2 doi: 10.1034/j.1398-9995.2003.00195.x – ident: e_1_2_13_38_2 doi: 10.1067/mai.2002.120954 – ident: e_1_2_13_48_2 doi: 10.1034/j.1398-9995.2001.00296.x – volume: 120 start-page: 729 year: 2007 ident: e_1_2_13_58_2 article-title: Basophil secretion in chronic urticaria publication-title: autoantibody-dependent or not? – ident: e_1_2_13_27_2 doi: 10.1111/1523-1747.ep12277582 – ident: e_1_2_13_42_2 doi: 10.1016/j.jaci.2005.12.1343 – volume: 75 start-page: 484 year: 1995 ident: e_1_2_13_70_2 article-title: Pseudoallergen‐free diet in the treatment of chronic urticaria. A prospective study publication-title: Acta Derm Venereol doi: 10.2340/0001555575484487 – ident: e_1_2_13_22_2 doi: 10.1046/j.1365-2133.2001.04175.x – ident: e_1_2_13_71_2 doi: 10.1016/S1382-6689(97)10050-3 – ident: e_1_2_13_39_2 doi: 10.4049/jimmunol.155.6.3152 – ident: e_1_2_13_49_2 doi: 10.1016/S0091-6749(95)70055-2 – volume: 96 start-page: 341 year: 2006 ident: e_1_2_13_63_2 article-title: Autoantibodies to the high‐affinity IgE receptor in children with chronic urticaria publication-title: J Allergy Clin Immunol – ident: e_1_2_13_65_2 doi: 10.1007/978-3-642-85267-1_2 – ident: e_1_2_13_77_2 doi: 10.1201/b13958-15 – volume: 96 start-page: 2606 year: 1995 ident: e_1_2_13_6_2 article-title: Serum IgG autoantibodies directed against the alpha chain of Fc epsilon RI publication-title: a selective marker and pathogenetic factor for a distinct subset of chronic urticaria patients? – ident: e_1_2_13_60_2 doi: 10.1016/0140-6736(92)90666-Q – volume: 61 start-page: 321 year: 2006 ident: e_1_2_13_79_2 article-title: EAACI/GA2LEN/EDF guideline publication-title: management of urticaria – volume: 4 start-page: 286 year: 1999 ident: e_1_2_13_19_2 article-title: Autoimmunity and the etiology of chronic urticaria publication-title: Can J Allergy Clin Immunol – volume: 78 start-page: 914 year: 1986 ident: e_1_2_13_47_2 article-title: Studies of the cellular infiltrate of chronic idiopathic urticaria publication-title: prominence of T-lymphocytes, monocytes, and mast cells – ident: e_1_2_13_21_2 doi: 10.1067/mai.2003.1605 – ident: e_1_2_13_80_2 doi: 10.1111/j.1365-2222.2006.02494.x – ident: e_1_2_13_75_2 doi: 10.1027/0838-1925.13.1.23 – ident: e_1_2_13_55_2 doi: 10.1159/000023902 – ident: e_1_2_13_67_2 doi: 10.1111/j.1365-2133.1975.tb06732.x – volume: 12 start-page: 311 year: 1999 ident: e_1_2_13_59_2 article-title: Autoimmune urticaria publication-title: Adv Dermatol – ident: e_1_2_13_56_2 doi: 10.1046/j.1523-1747.2002.01733.x – ident: e_1_2_13_31_2 doi: 10.1111/j.1365-2222.1991.tb03198.x – volume: 84 start-page: 66 year: 1989 ident: e_1_2_13_18_2 article-title: Syndrome of idiopathic chronic urticaria and angioedema with thyroid autoimmunity publication-title: a study of 90 patients – ident: e_1_2_13_68_2 doi: 10.1016/S0140-6736(86)90423-X – ident: e_1_2_13_34_2 doi: 10.1172/JCI511 – ident: e_1_2_13_23_2 doi: 10.1046/j.1365-2133.1999.02815.x – ident: e_1_2_13_62_2 doi: 10.1007/3-211-27377-8_15 – ident: e_1_2_13_50_2 doi: 10.1016/0091-6749(83)90096-9 – ident: e_1_2_13_12_2 doi: 10.1111/j.1365-2222.2005.02212.x – ident: e_1_2_13_66_2 doi: 10.1111/j.1365-2133.1973.tb08014.x – volume: 145 start-page: 815 year: 2005 ident: e_1_2_13_35_2 article-title: Isolation of the pathogenic IgG subclasses in chronic autoimmune urticaria publication-title: evidence that IgG1, IgG3, and IgG4 contain antireceptor antibodies that activate basophils while IgG2 is inactive – ident: e_1_2_13_13_2 doi: 10.1016/j.jaci.2006.09.035 – ident: e_1_2_13_28_2 doi: 10.1126/science.7542803 – volume: 138 start-page: 235 year: 2005 ident: e_1_2_13_74_2 article-title: Food‐additive‐induced urticaria publication-title: a survey of 838 patients with recurrent chronic idiopathic urticaria – ident: e_1_2_13_7_2 doi: 10.1016/S0091-6749(97)70071-X – volume: 114 start-page: 465 year: 2004 ident: e_1_2_13_3_2 article-title: Chronic urticaria publication-title: pathogenesis and treatment – volume: 133 start-page: 3282 year: 1984 ident: e_1_2_13_46_2 article-title: Thrombin‐induced degranulation of cultured bone marrow‐derived mast cells publication-title: J Immunol doi: 10.4049/jimmunol.133.6.3282 – ident: e_1_2_13_72_2 doi: 10.1067/mai.2002.121309 – ident: e_1_2_13_26_2 doi: 10.1111/1523-1747.ep12462239 – volume: 92 start-page: 132 issue: 1 year: 1993 ident: e_1_2_13_29_2 article-title: Chronic idiopathic urticaria publication-title: possible contribution of histamine-releasing factor to pathogenesis – ident: e_1_2_13_9_2 doi: 10.1111/j.1365-2222.1974.tb01384.x – volume: 163 start-page: 3976 year: 1999 ident: e_1_2_13_54_2 article-title: C‐C chemokines in allergen‐induced late‐phase cutaneous responses in atopic subjects publication-title: association of eotaxin with early 6-hour eosinophils, and of eotaxin-2 and monocyte chemoattractant protein-4 with the later 24-hour tissue eosinophilia, and relationship to basophils and other C-C chemokines (monocyte chemoattractant protein-3 and RANTES) – ident: e_1_2_13_16_2 doi: 10.1111/j.1398-9995.1962.tb02937.x |
| SSID | ssj0003598 |
| Score | 2.4273715 |
| SecondaryResourceType | review_article |
| Snippet | Summary
Chronic urticaria is defined as the presence of urticaria (hives) for at least 6 weeks with the assumption that it occurs daily or close to it. If we... Chronic urticaria is defined as the presence of urticaria (hives) for at least 6 weeks with the assumption that it occurs daily or close to it. If we eliminate... SummaryChronic urticaria is defined as the presence of urticaria (hives) for at least 6 weeks with the assumption that it occurs daily or close to it. If we... |
| SourceID | proquest pubmed pascalfrancis crossref wiley istex |
| SourceType | Aggregation Database Index Database Enrichment Source Publisher |
| StartPage | 777 |
| SubjectTerms | Allergic diseases Antibodies, Anti-Idiotypic - immunology Antibodies, Anti-Idiotypic - metabolism Autoantibodies - blood Autoimmunity Basophils - immunology Basophils - metabolism Biological and medical sciences Cell Degranulation - immunology Chronic Disease Fundamental and applied biological sciences. Psychology Fundamental immunology Histamine - immunology Histamine - metabolism Humans Immunoglobulin E - blood Immunopathology Mast Cells - immunology Mast Cells - metabolism Medical sciences Skin - immunology Skin - pathology Skin allergic diseases. Stinging insect allergies Thyroglobulin - immunology Thyroglobulin - metabolism Thyroid Gland - immunology Thyroid Gland - metabolism Urticaria - immunology Urticaria - pathology |
| Title | Pathogenesis of chronic urticaria |
| URI | https://api.istex.fr/ark:/67375/WNG-C4DBXWRS-L/fulltext.pdf https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1365-2222.2009.03256.x https://www.ncbi.nlm.nih.gov/pubmed/19400905 https://www.proquest.com/docview/20584641 https://www.proquest.com/docview/67371203 |
| Volume | 39 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1LT9wwEB4hKhCXlkehKa8gVdyyShw7sY-w5SHUIkRB7M2ynQShrXYrdlei_fWdibNLg0BCFTlFSSZOJjOez_bkG4AvCBFclskiQkczEWdlHElpiPdWMSvjKpU-2-I8O73mZz3Ra_Kf6F8Yzw8xm3Ajz6j7a3JwY0dtJ68ztHBraCdTDN8dwpN0gvDR5SOTFBHVedo9HuVS8XZSz7M3akWqd6T0B8qcNCNUXuWrXjwHS9sotw5Txx-gP31Bn53S70zGtuP-POF-fBsNLMP7Bs2GB978VmCuHKzCgq9v-XsVFr83K_drsHeBUHN4Sz3r3SgcVqHzrLzhhGRxwG4-wvXx0VX3NGrKM0ROIOiLrOGVEq6ULC9VmuDIzibWSuwiDKuKQubGEn8X4gEnEEQoxXLEIknGiqySeD5dh_nBcFB-gpBLI0WVOWk454VlxlqunBKiwBCLxwPIp59Cu4a7nEpo_NT_jGFQF5p0QZU1la51oR8CSGaSvzx_xytk9uuvPRMw933Kf8uFvjk_0V3-9bB3c_lDfwtgp2UOMwHioYtzlgawO7UPjW5LazFmUA4nI2yPkB9PXr6CGkxYjPfY8Ib1-PxUzF7FIoCsNo9Xv5juHh3Q3uf_FdyEJb-aRrNQWzA_vp-U2wjKxnandre_ibMhfA |
| linkProvider | Wiley-Blackwell |
| linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV3fT9swED5NoDFe2MYGZD8gSNPeUiWOndiPrMC6USrEQPTNsp1kmkAtoq0E--t3F6dlmZiEpuUpSnJxfL6zP9uX7wA-IERwWSaLCB3NRJyVcSSlId5bxayMq1T6aItB1jvnX4di2KQDon9hPD_EYsGNPKPur8nBaUG67eV1iBYeDe9kiuN3BwHlMiX4JiL9_dN7LimiqvPEezzKpeLtsJ4H39Qaq5ZJ7bcUO2kmqL7K5714CJi2cW49UB0-h6t5FX18ymVnNrUd9_MP9sf_pIMXsNYA2nDPW-BLeFKO1uGpT3F5tw4rx83m_SvYPUG0Of5OneuPSTiuQueJecMZyeKc3byG88ODs24vajI0RE4g7ous4ZUSrpQsL1Wa4OTOJtZK7CUMq4pC5sYShRdCAicQRyjFcoQjScaKrJJ4P92ApdF4VG5ByKWRosqcNJzzwjJjLVdOCVHgKIvXA8jnbaFdQ19OWTSu9G_TGNSFJl1Qck2la13o2wCSheS1p_B4hMzHurkXAubmkkLgcqEvBp91l-9_Gl6cftP9ALZb9rAQICq6OGdpADtzA9HoubQdY0bleDbB8gj88eTvT1CBCYvxHZvesu6_n_LZq1gEkNX28eiK6e7BHp29-VfBHXjWOzvu6_6XwdFbWPWba7Qo9Q6Wpjez8j1itKndrn3vF7gUJZg |
| linkToPdf | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV3fT9swED4hEGgvbGO_MjYIEtpbqsSxE_uRtXRsQIXYEH2zbCeZpqIW0VZi--u5i9OyTExC0_IUJbk4Pt_Zn-3LdwD7CBFclskiQkczEWdlHElpiPdWMSvjKpU-2mKQHV3wL0MxbOKf6F8Yzw-xXHAjz6j7a3Lw66JqO3kdoYVHQzuZ4vDdQTy5xrNYURqH3vk9lRQx1XnePR7lUvF2VM-Db2oNVWuk9VsKnTRT1F7l0148hEvbMLcep_pPYbSooQ9PGXXmM9txv_4gf_w_KngGmw2cDQ-8_T2HlXK8Bes-weXPLdg4bbbuX8DeGWLNyXfqWn9Mw0kVOk_LG85JFmfs5iVc9A-_dY-iJj9D5ASivsgaXinhSsnyUqUJTu1sYq3EPsKwqihkbiwReCEgcAJRhFIsRzCSZKzIKon301ewOp6MyzcQcmmkqDInDee8sMxYy5VTQhQ4xuL1APJFU2jXkJdTDo0r_dskBnWhSReUWlPpWhf6NoBkKXntCTweIfOhbu2lgLkZUQBcLvTl4JPu8t7H4eX5V30SwE7LHJYCREQX5ywNYHdhHxr9ljZjzLiczKdYHkE_nvz9CSowYTG-47U3rPvvp2z2KhYBZLV5PLpiunt4QGdv_1VwFzbOen198nlwvA1P_M4arUi9g9XZzbx8jwBtZndqz7sDCZ4kRw |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Pathogenesis+of+chronic+urticaria&rft.jtitle=Clinical+and+experimental+allergy&rft.au=Kaplan%2C+AP&rft.au=Greaves%2C+M&rft.date=2009-06-01&rft.issn=0954-7894&rft.eissn=1365-2222&rft.volume=39&rft.issue=6&rft.spage=777&rft.epage=787&rft_id=info:doi/10.1111%2Fj.1365-2222.2009.03256.x&rft.externalDBID=NO_FULL_TEXT |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0954-7894&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0954-7894&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0954-7894&client=summon |