IL3 effect on basophils histamine release upon stimulation with chronic urticaria sera
Background: Chronic urticaria is thought to be an autoimmune disorder in 35–40% of patients because of the presence of an immunoglobulin G (IgG) antibody reactive with the IgE receptor. Patients possessing this antibody are identified by the ability of serum to degranulate donor basophils to releas...
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Published in | Allergy (Copenhagen) Vol. 58; no. 8; pp. 802 - 807 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Munksgaard International Publishers
01.08.2003
Blackwell |
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Abstract | Background: Chronic urticaria is thought to be an autoimmune disorder in 35–40% of patients because of the presence of an immunoglobulin G (IgG) antibody reactive with the IgE receptor. Patients possessing this antibody are identified by the ability of serum to degranulate donor basophils to release histamine. We questioned whether priming of basophils with interleukin 3 (IL3) would facilitate identification of patients and/or alter the percentage of patients who have a positive assay.
Methods: We incubated 37 chronic urticaria sera with basophils from donors with no urticaria with and without priming with IL3 and compared histamine release in each instance. We also preincubated basophils from a ‘non‐releaser’ with IL3, used these cells to assay chronic urticaria sera, and assessed the contribution of complement.
Results: Interleukin 3 increases the amount of histamine release by the sera which is able to activate basophils, but it does not convert negative sera into positive releasers. Interleukin 3 is able to partially reverse ‘non‐releaser’ basophils into cells that respond to chronic urticaria sera, and complement cannot account for the augmentation seen.
Conclusions: Preincubating basophils with IL3 facilitates the identification of sera with anti‐IgE receptor antibody but does not affect the percentage of sera designated as positive. |
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AbstractList | Background: Chronic urticaria is thought to be an autoimmune disorder in 35–40% of patients because of the presence of an immunoglobulin G (IgG) antibody reactive with the IgE receptor. Patients possessing this antibody are identified by the ability of serum to degranulate donor basophils to release histamine. We questioned whether priming of basophils with interleukin 3 (IL3) would facilitate identification of patients and/or alter the percentage of patients who have a positive assay.
Methods: We incubated 37 chronic urticaria sera with basophils from donors with no urticaria with and without priming with IL3 and compared histamine release in each instance. We also preincubated basophils from a ‘non‐releaser’ with IL3, used these cells to assay chronic urticaria sera, and assessed the contribution of complement.
Results: Interleukin 3 increases the amount of histamine release by the sera which is able to activate basophils, but it does not convert negative sera into positive releasers. Interleukin 3 is able to partially reverse ‘non‐releaser’ basophils into cells that respond to chronic urticaria sera, and complement cannot account for the augmentation seen.
Conclusions: Preincubating basophils with IL3 facilitates the identification of sera with anti‐IgE receptor antibody but does not affect the percentage of sera designated as positive. BACKGROUNDChronic urticaria is thought to be an autoimmune disorder in 35-40% of patients because of the presence of an immunoglobulin G (IgG) antibody reactive with the IgE receptor. Patients possessing this antibody are identified by the ability of serum to degranulate donor basophils to release histamine. We questioned whether priming of basophils with interleukin 3 (IL3) would facilitate identification of patients and/or alter the percentage of patients who have a positive assay.METHODSWe incubated 37 chronic urticaria sera with basophils from donors with no urticaria with and without priming with IL3 and compared histamine release in each instance. We also preincubated basophils from a 'non-releaser' with IL3, used these cells to assay chronic urticaria sera, and assessed the contribution of complement.RESULTSInterleukin 3 increases the amount of histamine release by the sera which is able to activate basophils, but it does not convert negative sera into positive releasers. Interleukin 3 is able to partially reverse 'non-releaser' basophils into cells that respond to chronic urticaria sera, and complement cannot account for the augmentation seen.CONCLUSIONSPreincubating basophils with IL3 facilitates the identification of sera with anti-IgE receptor antibody but does not affect the percentage of sera designated as positive. Background: Chronic urticaria is thought to be an autoimmune disorder in 35-40% of patients because of the presence of an immunoglobulin G (IgG) antibody reactive with the IgE receptor. Patients possessing this antibody are identified by the ability of serum to degranulate donor basophils to release histamine. We questioned whether priming of basophils with interleukin 3 (IL3) would facilitate identification of patients and/or alter the percentage of patients who have a positive assay. Methods: We incubated 37 chronic urticaria sera with basophils from donors with no urticaria with and without priming with IL3 and compared histamine release in each instance. We also preincubated basophils from a `non-releaser' with IL3, used these cells to assay chronic urticaria sera, and assessed the contribution of complement. Results: Interleukin 3 increases the amount of histamine release by the sera which is able to activate basophils, but it does not convert negative sera into positive releasers. Interleukin 3 is able to partially reverse `non-releaser' basophils into cells that respond to chronic urticaria sera, and complement cannot account for the augmentation seen. Conclusions: Preincubating basophils with IL3 facilitates the identification of sera with anti-IgE receptor antibody but does not affect the percentage of sera designated as positive. Chronic urticaria is thought to be an autoimmune disorder in 35-40% of patients because of the presence of an immunoglobulin G (IgG) antibody reactive with the IgE receptor. Patients possessing this antibody are identified by the ability of serum to degranulate donor basophils to release histamine. We questioned whether priming of basophils with interleukin 3 (IL3) would facilitate identification of patients and/or alter the percentage of patients who have a positive assay. We incubated 37 chronic urticaria sera with basophils from donors with no urticaria with and without priming with IL3 and compared histamine release in each instance. We also preincubated basophils from a 'non-releaser' with IL3, used these cells to assay chronic urticaria sera, and assessed the contribution of complement. Interleukin 3 increases the amount of histamine release by the sera which is able to activate basophils, but it does not convert negative sera into positive releasers. Interleukin 3 is able to partially reverse 'non-releaser' basophils into cells that respond to chronic urticaria sera, and complement cannot account for the augmentation seen. Preincubating basophils with IL3 facilitates the identification of sera with anti-IgE receptor antibody but does not affect the percentage of sera designated as positive. Background: Chronic urticaria is thought to be an autoimmune disorder in 35–40% of patients because of the presence of an immunoglobulin G (IgG) antibody reactive with the IgE receptor. Patients possessing this antibody are identified by the ability of serum to degranulate donor basophils to release histamine. We questioned whether priming of basophils with interleukin 3 (IL3) would facilitate identification of patients and/or alter the percentage of patients who have a positive assay. Methods: We incubated 37 chronic urticaria sera with basophils from donors with no urticaria with and without priming with IL3 and compared histamine release in each instance. We also preincubated basophils from a ‘non‐releaser’ with IL3, used these cells to assay chronic urticaria sera, and assessed the contribution of complement. Results: Interleukin 3 increases the amount of histamine release by the sera which is able to activate basophils, but it does not convert negative sera into positive releasers. Interleukin 3 is able to partially reverse ‘non‐releaser’ basophils into cells that respond to chronic urticaria sera, and complement cannot account for the augmentation seen. Conclusions: Preincubating basophils with IL3 facilitates the identification of sera with anti‐IgE receptor antibody but does not affect the percentage of sera designated as positive. |
Author | Ferrer, M. Kaplan, A. P. Luquin, E. |
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Keywords | Human Immunopathology Skin disease Urticaria basophils; IgE receptor IgE Cytokine Granulocyte Immunoglobulin receptor Basophil Histamine Interleukin 3 IL3; urticaria |
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References | 2001; 144 1991; 266 1993; 328 1997; 99 1991; 21 2000; 23 2000; 55 2000; 164 2000; 165 2002; 109 2001; 107 1999; 104 1998; 101 1996; 97 1996; 106 e_1_2_11_13_2 e_1_2_11_9_2 e_1_2_11_12_2 e_1_2_11_8_2 e_1_2_11_11_2 e_1_2_11_7_2 e_1_2_11_10_2 e_1_2_11_6_2 e_1_2_11_17_2 e_1_2_11_5_2 e_1_2_11_16_2 e_1_2_11_4_2 e_1_2_11_15_2 e_1_2_11_3_2 Riske F (e_1_2_11_14_2) 1991; 266 e_1_2_11_2_2 |
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Snippet | Background: Chronic urticaria is thought to be an autoimmune disorder in 35–40% of patients because of the presence of an immunoglobulin G (IgG) antibody... Chronic urticaria is thought to be an autoimmune disorder in 35-40% of patients because of the presence of an immunoglobulin G (IgG) antibody reactive with the... Background: Chronic urticaria is thought to be an autoimmune disorder in 35–40% of patients because of the presence of an immunoglobulin G (IgG) antibody... Background: Chronic urticaria is thought to be an autoimmune disorder in 35-40% of patients because of the presence of an immunoglobulin G (IgG) antibody... BACKGROUNDChronic urticaria is thought to be an autoimmune disorder in 35-40% of patients because of the presence of an immunoglobulin G (IgG) antibody... |
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SubjectTerms | Adult Allergic diseases basophils Basophils - metabolism Biological and medical sciences Chronic Disease Female histamine Histamine Release - drug effects Humans IgE receptor IL3 Immunopathology In Vitro Techniques Interleukin-3 - pharmacology Male Medical sciences Skin allergic diseases. Stinging insect allergies urticaria Urticaria - blood |
Title | IL3 effect on basophils histamine release upon stimulation with chronic urticaria sera |
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