Leukocyte-Derived IFN-α/β and Epithelial IFN-λ Constitute a Compartmentalized Mucosal Defense System that Restricts Enteric Virus Infections
Epithelial cells are a major port of entry for many viruses, but the molecular networks which protect barrier surfaces against viral infections are incompletely understood. Viral infections induce simultaneous production of type I (IFN-α/β) and type III (IFN-λ) interferons. All nucleated cells are b...
Saved in:
| Published in | PLoS pathogens Vol. 11; no. 4; p. e1004782 |
|---|---|
| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Public Library of Science
01.04.2015
Public Library of Science (PLoS) |
| Subjects | |
| Online Access | Get full text |
Cover
Loading…
| Abstract | Epithelial cells are a major port of entry for many viruses, but the molecular networks which protect barrier surfaces against viral infections are incompletely understood. Viral infections induce simultaneous production of type I (IFN-α/β) and type III (IFN-λ) interferons. All nucleated cells are believed to respond to IFN-α/β, whereas IFN-λ responses are largely confined to epithelial cells. We observed that intestinal epithelial cells, unlike hematopoietic cells of this organ, express only very low levels of functional IFN-α/β receptors. Accordingly, after oral infection of IFN-α/β receptor-deficient mice, human reovirus type 3 specifically infected cells in the lamina propria but, strikingly, did not productively replicate in gut epithelial cells. By contrast, reovirus replicated almost exclusively in gut epithelial cells of IFN-λ receptor-deficient mice, suggesting that the gut mucosa is equipped with a compartmentalized IFN system in which epithelial cells mainly respond to IFN-λ that they produce after viral infection, whereas other cells of the gut mostly rely on IFN-α/β for antiviral defense. In suckling mice with IFN-λ receptor deficiency, reovirus replicated in the gut epithelium and additionally infected epithelial cells lining the bile ducts, indicating that infants may use IFN-λ for the control of virus infections in various epithelia-rich tissues. Thus, IFN-λ should be regarded as an autonomous virus defense system of the gut mucosa and other epithelial barriers that may have evolved to avoid unnecessarily frequent triggering of the IFN-α/β system which would induce exacerbated inflammation. |
|---|---|
| AbstractList | Epithelial cells are a major port of entry for many viruses, but the molecular networks which protect barrier surfaces against viral infections are incompletely understood. Viral infections induce simultaneous production of type I (IFN-α/β) and type III (IFN-λ) interferons. All nucleated cells are believed to respond to IFN-α/β, whereas IFN-λ responses are largely confined to epithelial cells. We observed that intestinal epithelial cells, unlike hematopoietic cells of this organ, express only very low levels of functional IFN-α/β receptors. Accordingly, after oral infection of IFN-α/β receptor-deficient mice, human reovirus type 3 specifically infected cells in the lamina propria but, strikingly, did not productively replicate in gut epithelial cells. By contrast, reovirus replicated almost exclusively in gut epithelial cells of IFN-λ receptor-deficient mice, suggesting that the gut mucosa is equipped with a compartmentalized IFN system in which epithelial cells mainly respond to IFN-λ that they produce after viral infection, whereas other cells of the gut mostly rely on IFN-α/β for antiviral defense. In suckling mice with IFN-λ receptor deficiency, reovirus replicated in the gut epithelium and additionally infected epithelial cells lining the bile ducts, indicating that infants may use IFN-λ for the control of virus infections in various epithelia-rich tissues. Thus, IFN-λ should be regarded as an autonomous virus defense system of the gut mucosa and other epithelial barriers that may have evolved to avoid unnecessarily frequent triggering of the IFN-α/β system which would induce exacerbated inflammation. Epithelial cells are a major port of entry for many viruses, but the molecular networks which protect barrier surfaces against viral infections are incompletely understood. Viral infections induce simultaneous production of type I (IFN-α/β) and type III (IFN-λ) interferons. All nucleated cells are believed to respond to IFN-α/β, whereas IFN-λ responses are largely confined to epithelial cells. We observed that intestinal epithelial cells, unlike hematopoietic cells of this organ, express only very low levels of functional IFN-α/β receptors. Accordingly, after oral infection of IFN-α/β receptor-deficient mice, human reovirus type 3 specifically infected cells in the lamina propria but, strikingly, did not productively replicate in gut epithelial cells. By contrast, reovirus replicated almost exclusively in gut epithelial cells of IFN-λ receptor-deficient mice, suggesting that the gut mucosa is equipped with a compartmentalized IFN system in which epithelial cells mainly respond to IFN-λ that they produce after viral infection, whereas other cells of the gut mostly rely on IFN-α/β for antiviral defense. In suckling mice with IFN-λ receptor deficiency, reovirus replicated in the gut epithelium and additionally infected epithelial cells lining the bile ducts, indicating that infants may use IFN-λ for the control of virus infections in various epithelia-rich tissues. Thus, IFN-λ should be regarded as an autonomous virus defense system of the gut mucosa and other epithelial barriers that may have evolved to avoid unnecessarily frequent triggering of the IFN-α/β system which would induce exacerbated inflammation. Virus-induced interferon consists of two distinct families of molecules, IFN-α/β and IFN-λ. IFN-α/β family members are key antiviral molecules that confer protection against a large number of viruses infecting a wide variety of cell types. By contrast, IFN-λ responses are largely confined to epithelial cells due to highly restricted expression of the cognate receptor. Interestingly, virus resistance of the gut epithelium is not dependent on IFN-α/β but rather relies on IFN-λ, questioning the prevailing view that receptors for IFN-α/β are expressed ubiquitously. Here we demonstrate that the IFN-α/β system is unable to compensate for IFN-λ deficiency during infections with epitheliotropic viruses because intestinal epithelial cells do not express functional receptors for IFN-α/β. We further demonstrate that virus-infected intestinal epithelial cells are potent producers of IFN-λ, indicating that the gut mucosa possesses a compartmentalized IFN system in which epithelial cells predominantly respond to IFN-λ, whereas other cells of the gut mainly rely on IFN-α/β for antiviral defense. We suggest that IFN-λ may have evolved as an autonomous virus defense system of the gut mucosa to avoid unnecessarily frequent triggering of the IFN-α/β system which, due to its potent activity on immune cells, would induce exacerbated inflammation. Epithelial cells are a major port of entry for many viruses, but the molecular networks which protect barrier surfaces against viral infections are incompletely understood. Viral infections induce simultaneous production of type I (IFN-α/β) and type III (IFN-λ) interferons. All nucleated cells are believed to respond to IFN-α/β, whereas IFN-λ responses are largely confined to epithelial cells. We observed that intestinal epithelial cells, unlike hematopoietic cells of this organ, express only very low levels of functional IFN-α/β receptors. Accordingly, after oral infection of IFN-α/β receptor-deficient mice, human reovirus type 3 specifically infected cells in the lamina propria but, strikingly, did not productively replicate in gut epithelial cells. By contrast, reovirus replicated almost exclusively in gut epithelial cells of IFN-λ receptor-deficient mice, suggesting that the gut mucosa is equipped with a compartmentalized IFN system in which epithelial cells mainly respond to IFN-λ that they produce after viral infection, whereas other cells of the gut mostly rely on IFN-α/β for antiviral defense. In suckling mice with IFN-λ receptor deficiency, reovirus replicated in the gut epithelium and additionally infected epithelial cells lining the bile ducts, indicating that infants may use IFN-λ for the control of virus infections in various epithelia-rich tissues. Thus, IFN-λ should be regarded as an autonomous virus defense system of the gut mucosa and other epithelial barriers that may have evolved to avoid unnecessarily frequent triggering of the IFN-α/β system which would induce exacerbated inflammation.Epithelial cells are a major port of entry for many viruses, but the molecular networks which protect barrier surfaces against viral infections are incompletely understood. Viral infections induce simultaneous production of type I (IFN-α/β) and type III (IFN-λ) interferons. All nucleated cells are believed to respond to IFN-α/β, whereas IFN-λ responses are largely confined to epithelial cells. We observed that intestinal epithelial cells, unlike hematopoietic cells of this organ, express only very low levels of functional IFN-α/β receptors. Accordingly, after oral infection of IFN-α/β receptor-deficient mice, human reovirus type 3 specifically infected cells in the lamina propria but, strikingly, did not productively replicate in gut epithelial cells. By contrast, reovirus replicated almost exclusively in gut epithelial cells of IFN-λ receptor-deficient mice, suggesting that the gut mucosa is equipped with a compartmentalized IFN system in which epithelial cells mainly respond to IFN-λ that they produce after viral infection, whereas other cells of the gut mostly rely on IFN-α/β for antiviral defense. In suckling mice with IFN-λ receptor deficiency, reovirus replicated in the gut epithelium and additionally infected epithelial cells lining the bile ducts, indicating that infants may use IFN-λ for the control of virus infections in various epithelia-rich tissues. Thus, IFN-λ should be regarded as an autonomous virus defense system of the gut mucosa and other epithelial barriers that may have evolved to avoid unnecessarily frequent triggering of the IFN-α/β system which would induce exacerbated inflammation. |
| Author | Hernandez, Pedro Gronke, Konrad Diefenbach, Andreas Staeheli, Peter Mahlakõiv, Tanel |
| AuthorAffiliation | 2 Spemann Graduate School of Biology and Medicine (SGBM), Albert Ludwigs University Freiburg, Freiburg, Germany Stanford University, UNITED STATES 1 Institute of Virology, University Medical Center Freiburg, Freiburg, Germany 5 Research Centre Immunology and Institute of Medical Microbiology and Hygiene, University of Mainz Medical Centre, Mainz, Germany 3 Institute of Medical Microbiology and Hygiene, University Medical Center Freiburg, Freiburg, Germany 4 International Max Planck Research School for Molecular and Cell Biology (IMPRS-MCB), Freiburg, Germany |
| AuthorAffiliation_xml | – name: 1 Institute of Virology, University Medical Center Freiburg, Freiburg, Germany – name: 4 International Max Planck Research School for Molecular and Cell Biology (IMPRS-MCB), Freiburg, Germany – name: 3 Institute of Medical Microbiology and Hygiene, University Medical Center Freiburg, Freiburg, Germany – name: 5 Research Centre Immunology and Institute of Medical Microbiology and Hygiene, University of Mainz Medical Centre, Mainz, Germany – name: Stanford University, UNITED STATES – name: 2 Spemann Graduate School of Biology and Medicine (SGBM), Albert Ludwigs University Freiburg, Freiburg, Germany |
| Author_xml | – sequence: 1 givenname: Tanel surname: Mahlakõiv fullname: Mahlakõiv, Tanel – sequence: 2 givenname: Pedro surname: Hernandez fullname: Hernandez, Pedro – sequence: 3 givenname: Konrad surname: Gronke fullname: Gronke, Konrad – sequence: 4 givenname: Andreas surname: Diefenbach fullname: Diefenbach, Andreas – sequence: 5 givenname: Peter surname: Staeheli fullname: Staeheli, Peter |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25849543$$D View this record in MEDLINE/PubMed |
| BookMark | eNp9kstu1DAUhiNURC_wBgh5ySZTO3YShwUSmk7LSANI3LaWxz7peEjs1HYqDS_Bs5Qt79BnwsNMUcuClW__-X6d4_84O7DOQpY9J3hCaE1O1270VnaTYZBxQjBmNS8eZUekLGle05od3NsfZschrJOGUFI9yQ6LkrOmZPQo-7GA8ZtTmwj5GXhzDRrNz9_ntzentz-RtBrNBhNX0BnZ7R5-oamzIZo4RkAyHfpB-tiDjbIz31P5u1G5kNRn0IINgD5tQoQexZWM6COE6I2KAc1sTHYKfTV-DGhuW1DRJPDT7HEruwDP9utJ9uV89nn6Nl98uJhP3yxyxWoWcwKM6Yq3RatYtdRcV5gVijQcdMNVg3VbUgZFTRrQULeyIVgWS90STglrOaUn2XzH1U6uxeBNL_1GOGnEnwvnL0Vqy6gORFVyJeumIoQwhqnmBWmIKlSC4QazMrFe71jDuOxBqzQLL7sH0Icv1qzEpbsWjHLOapwAL_cA767GNCPRm6Cg66QFNwZBqrrAqYWySdIX973-mtz9aBK82gmUdyF4aIUyUW5nm6xNJwgW2_iIfXzENj5iH59UzP4pvuP_t-w3bl7SCA |
| CitedBy_id | crossref_primary_10_1089_jir_2019_0009 crossref_primary_10_3389_fimmu_2016_00598 crossref_primary_10_1186_s12934_024_02397_y crossref_primary_10_1016_j_coi_2024_102456 crossref_primary_10_1128_JVI_02079_16 crossref_primary_10_3389_fimmu_2023_1250541 crossref_primary_10_1099_jgv_0_000522 crossref_primary_10_1007_s00705_018_4087_0 crossref_primary_10_1016_j_antiviral_2017_10_017 crossref_primary_10_1038_s41590_019_0345_x crossref_primary_10_4049_jimmunol_2100707 crossref_primary_10_1016_j_jcmgh_2019_02_007 crossref_primary_10_3389_fimmu_2024_1441908 crossref_primary_10_3390_ijms22094726 crossref_primary_10_1038_s41577_019_0182_z crossref_primary_10_3389_fimmu_2021_637399 crossref_primary_10_3389_fimmu_2018_03086 crossref_primary_10_1016_j_it_2018_08_008 crossref_primary_10_1128_mbio_01308_22 crossref_primary_10_3389_fimmu_2017_01707 crossref_primary_10_1007_s00005_019_00564_3 crossref_primary_10_1126_sciimmunol_abd5318 crossref_primary_10_3342_kjorl_hns_2015_58_11_739 crossref_primary_10_1016_j_cytogfr_2016_02_005 crossref_primary_10_3389_fimmu_2017_00459 crossref_primary_10_1002_eji_201646519 crossref_primary_10_4049_immunohorizons_2200025 crossref_primary_10_1080_2162402X_2023_2209473 crossref_primary_10_1371_journal_pone_0230667 crossref_primary_10_1007_s00705_022_05461_3 crossref_primary_10_1016_j_celrep_2025_115243 crossref_primary_10_1016_j_ijbiomac_2024_136712 crossref_primary_10_1016_j_immuni_2019_03_025 crossref_primary_10_1128_jvi_00917_22 crossref_primary_10_1021_acs_jproteome_0c00164 crossref_primary_10_3389_fimmu_2017_01302 crossref_primary_10_3390_cells11244041 crossref_primary_10_1038_mi_2017_77 crossref_primary_10_1093_protein_gzy029 crossref_primary_10_3389_fimmu_2017_01661 crossref_primary_10_3390_v10010046 crossref_primary_10_1080_14760584_2021_1927724 crossref_primary_10_1016_j_chom_2019_04_005 crossref_primary_10_1016_j_coi_2024_102430 crossref_primary_10_1038_srep24530 crossref_primary_10_3389_fvets_2019_00034 crossref_primary_10_1016_j_coi_2018_10_007 crossref_primary_10_1016_j_ejps_2024_106974 crossref_primary_10_3390_pathogens12091142 crossref_primary_10_1186_s13567_024_01436_1 crossref_primary_10_1146_annurev_virology_110615_042152 crossref_primary_10_3389_fimmu_2019_02674 crossref_primary_10_1038_s41435_018_0028_x crossref_primary_10_1128_JVI_02167_20 crossref_primary_10_1016_j_cytogfr_2016_03_002 crossref_primary_10_1038_s41584_021_00606_1 crossref_primary_10_1016_j_chom_2017_08_021 crossref_primary_10_3389_fimmu_2017_01232 crossref_primary_10_3389_fimmu_2021_705342 crossref_primary_10_1016_j_micinf_2024_105466 crossref_primary_10_1084_jem_20160437 crossref_primary_10_1371_journal_ppat_1007420 crossref_primary_10_3389_fmicb_2021_806084 crossref_primary_10_1128_JVI_00480_20 crossref_primary_10_3389_fmicb_2018_02943 crossref_primary_10_1016_j_jconrel_2023_05_029 crossref_primary_10_1038_ni_3212 crossref_primary_10_1080_19490976_2024_2447830 crossref_primary_10_1371_journal_ppat_1008515 crossref_primary_10_3390_ijms221910851 crossref_primary_10_1038_s41467_021_22928_0 crossref_primary_10_1016_j_mucimm_2024_03_011 crossref_primary_10_1089_jir_2018_0046 crossref_primary_10_3389_fimmu_2021_793841 crossref_primary_10_1016_j_cell_2024_10_010 crossref_primary_10_1016_j_mucimm_2024_03_013 crossref_primary_10_7554_eLife_65762 crossref_primary_10_1016_j_smim_2019_101303 crossref_primary_10_1128_mbio_00550_24 crossref_primary_10_1002_eji_202048777 crossref_primary_10_3389_fimmu_2017_00671 crossref_primary_10_1101_cshperspect_a031674 crossref_primary_10_1155_2022_8873536 crossref_primary_10_1073_pnas_2409684121 crossref_primary_10_1128_JVI_00603_20 crossref_primary_10_4049_jimmunol_2000979 crossref_primary_10_1128_JVI_02000_18 crossref_primary_10_1016_j_drudis_2015_10_021 crossref_primary_10_1038_s41598_019_52307_1 crossref_primary_10_1128_mBio_02540_20 crossref_primary_10_1016_j_coi_2024_102412 crossref_primary_10_3390_jmp4040024 crossref_primary_10_1016_j_coi_2024_102413 crossref_primary_10_3390_v13040589 crossref_primary_10_1016_j_antiviral_2017_01_016 crossref_primary_10_1371_journal_ppat_1008986 crossref_primary_10_1128_jvi_01147_24 crossref_primary_10_7554_eLife_74072 crossref_primary_10_1089_jir_2019_0040 crossref_primary_10_1128_jvi_01388_22 crossref_primary_10_1089_vim_2020_0076 crossref_primary_10_1128_JVI_01073_19 crossref_primary_10_1099_jgv_0_001660 crossref_primary_10_1128_jvi_01705_21 crossref_primary_10_15252_msb_20209833 crossref_primary_10_3389_fimmu_2024_1338096 crossref_primary_10_1016_j_coi_2023_102400 crossref_primary_10_3390_v11110998 crossref_primary_10_1016_j_coi_2021_07_014 crossref_primary_10_1089_jir_2024_0107 crossref_primary_10_1128_jvi_00706_22 crossref_primary_10_3390_v12060667 crossref_primary_10_1128_JVI_01677_17 crossref_primary_10_1016_j_fsi_2018_12_008 crossref_primary_10_1146_annurev_virology_111821_112317 crossref_primary_10_1186_s12974_016_0551_5 crossref_primary_10_1371_journal_ppat_1008057 crossref_primary_10_3390_v12040405 crossref_primary_10_3390_v12091039 crossref_primary_10_1128_mbio_00443_22 crossref_primary_10_1002_eji_202048990 crossref_primary_10_1016_j_coi_2024_102424 crossref_primary_10_1089_jir_2019_0036 crossref_primary_10_3389_fimmu_2020_608645 crossref_primary_10_1146_annurev_immunol_101921_050835 crossref_primary_10_1074_jbc_R117_777102 crossref_primary_10_1186_s12967_024_05673_y crossref_primary_10_1128_mbio_01130_24 crossref_primary_10_1016_j_tim_2017_10_010 crossref_primary_10_1084_jem_20190295 crossref_primary_10_1073_pnas_1615422114 crossref_primary_10_1016_j_immuni_2017_04_027 crossref_primary_10_3389_fimmu_2017_00258 crossref_primary_10_1016_j_immuni_2017_04_025 crossref_primary_10_1084_jem_20181621 crossref_primary_10_1371_journal_pone_0247738 crossref_primary_10_1016_j_immuni_2015_07_001 crossref_primary_10_3389_fimmu_2017_00749 crossref_primary_10_1038_ni_3821 crossref_primary_10_1016_j_dci_2024_105236 crossref_primary_10_1089_jir_2023_0037 crossref_primary_10_1016_j_celrep_2017_10_059 crossref_primary_10_1038_gene_2016_24 crossref_primary_10_3389_fvets_2020_00045 crossref_primary_10_4049_jimmunol_1601430 crossref_primary_10_1053_j_gastro_2017_03_015 crossref_primary_10_3390_v15122284 crossref_primary_10_1016_j_virusres_2021_198342 crossref_primary_10_3390_microorganisms9010105 crossref_primary_10_1084_jem_20161289 crossref_primary_10_1016_j_ejpb_2022_02_006 crossref_primary_10_1371_journal_pone_0164858 crossref_primary_10_1016_j_jim_2017_03_001 crossref_primary_10_1089_jir_2024_0096 crossref_primary_10_3390_ijms23179661 crossref_primary_10_3389_fimmu_2017_00119 crossref_primary_10_1016_j_virusres_2016_09_001 crossref_primary_10_1128_mbio_02791_22 crossref_primary_10_1089_jir_2023_0040 crossref_primary_10_1016_j_virusres_2016_05_015 crossref_primary_10_1007_s40588_018_0079_9 crossref_primary_10_1099_jgv_0_001651 crossref_primary_10_1371_journal_ppat_1005600 crossref_primary_10_1038_s41392_024_02049_y crossref_primary_10_1089_jir_2023_0046 crossref_primary_10_3389_fimmu_2017_01281 crossref_primary_10_7554_eLife_37552 crossref_primary_10_7554_eLife_33354 crossref_primary_10_1016_j_chom_2020_02_003 crossref_primary_10_1371_journal_ppat_1005684 crossref_primary_10_3389_fgene_2022_976814 crossref_primary_10_1016_j_it_2016_06_003 crossref_primary_10_3389_fimmu_2018_01270 crossref_primary_10_1080_22221751_2023_2239937 |
| Cites_doi | 10.1016/j.immuni.2012.05.020 10.1016/j.exger.2004.06.013 10.1089/jir.2010.0061 10.1038/jid.2010.244 10.1126/science.1235214 10.1002/hep.24189 10.1371/journal.ppat.1000151 10.1053/j.gastro.2011.12.055 10.1172/JCI16303 10.1016/j.immuni.2012.04.011 10.1074/jbc.M608618200 10.1007/s13365-011-0038-1 10.1073/pnas.1100552108 10.1111/j.1398-9995.2008.01826.x 10.1128/JVI.00272-10 10.1073/pnas.1212188109 10.1056/NEJM198208193070806 10.1128/JVI.00391-08 10.1016/j.immuni.2012.03.013 10.1016/j.virusres.2011.07.011 10.2223/JPED.1608 10.1099/vir.0.83391-0 10.1099/0022-1317-68-3-945 10.1084/jem.20101664 10.2174/1568005310101020117 10.1006/viro.2002.1723 10.1016/S0952-7915(02)00349-7 10.1385/IR:23:2-3:229 10.1038/ni873 10.1126/science.1258100 10.1371/journal.ppat.1000017 10.1089/107999099313802 10.1002/hep.24580 10.1002/eji.200324610 10.1016/j.virol.2005.09.024 10.1371/journal.ppat.1003064 10.3109/13550280903586394 10.1111/j.1600-065X.1995.tb00090.x 10.1038/ni1303 10.1002/hep.510270603 10.1128/JVI.68.10.6458-6465.1994 10.1038/ni875 10.1371/journal.ppat.1002670 10.1006/viro.2002.1699 10.1099/vir.0.051276-0 10.1371/journal.ppat.1003773 10.4049/jimmunol.180.4.2474 10.1128/JVI.01956-12 10.1074/jbc.R700016200 10.1038/ni.2915 10.1128/JVI.02675-06 10.1038/nature09907 10.1016/j.pharmthera.2004.12.002 10.1084/jem.20061587 10.1007/978-1-60761-362-6_32 10.1128/JVI.01703-09 10.1126/science.8009221 10.1038/ncomms4864 10.1159/000360084 10.1038/35073080 10.3109/00313026909071296 10.1016/0882-4010(86)90034-3 10.1146/annurev.immunol.23.021704.115843 10.1371/journal.pone.0002961 10.4049/jimmunol.182.3.1296 10.1016/S0014-5793(99)01598-7 10.1128/JVI.68.12.8428-8432.1994 |
| ContentType | Journal Article |
| Copyright | 2015 Mahlakõiv et al 2015 Mahlakõiv et al |
| Copyright_xml | – notice: 2015 Mahlakõiv et al 2015 Mahlakõiv et al |
| DBID | AAYXX CITATION CGR CUY CVF ECM EIF NPM 7X8 5PM DOA |
| DOI | 10.1371/journal.ppat.1004782 |
| DatabaseName | CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic PubMed Central (Full Participant titles) DOAJ Directory of Open Access Journals |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic |
| DatabaseTitleList | MEDLINE MEDLINE - Academic |
| Database_xml | – sequence: 1 dbid: DOA name: DOAJ Directory of Open Access Journals url: https://www.doaj.org/ sourceTypes: Open Website – sequence: 2 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: 3 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 | Biology |
| DocumentTitleAlternate | Compartmentalized Mucosal Defense System |
| EISSN | 1553-7374 |
| ExternalDocumentID | oai_doaj_org_article_658ca7961114403d82191c2cf1809045 PMC4388470 25849543 10_1371_journal_ppat_1004782 |
| Genre | Research Support, Non-U.S. Gov't Journal Article |
| GroupedDBID | --- 123 29O 2WC 53G 5VS 7X7 88E 8FE 8FH 8FI 8FJ AAFWJ AAUCC AAWOE AAYXX ABDBF ABUWG ACGFO ACIHN ACPRK ACUHS ADBBV ADRAZ AEAQA AENEX AEUYN AFKRA AFPKN AFRAH AHMBA ALMA_UNASSIGNED_HOLDINGS AOIJS B0M BAWUL BBNVY BCNDV BENPR BHPHI BPHCQ BVXVI BWKFM CCPQU CITATION CS3 DIK DU5 E3Z EAP EAS EBD EMK EMOBN ESX F5P FPL FYUFA GROUPED_DOAJ GX1 HCIFZ HMCUK HYE IAO IHR INH INR ISN ISR ITC KQ8 LK8 M1P M48 M7P MM. O5R O5S OK1 OVT P2P PGMZT PHGZM PHGZT PIMPY PQQKQ PROAC PSQYO PV9 QF4 QN7 RNS RPM RZL SV3 TR2 TUS UKHRP WOW ~8M 3V. CGR CUY CVF ECM EIF H13 IPNFZ M~E NPM RIG WOQ 7X8 PPXIY PQGLB 5PM PJZUB PUEGO |
| ID | FETCH-LOGICAL-c474t-1e44d68f2fc46bd8d6042c198ed98c90df534e2719ede7fa910a2bdf18314f833 |
| IEDL.DBID | M48 |
| ISSN | 1553-7374 1553-7366 |
| IngestDate | Wed Aug 27 01:14:09 EDT 2025 Thu Aug 21 14:31:21 EDT 2025 Fri Jul 11 01:44:42 EDT 2025 Wed Feb 19 02:33:52 EST 2025 Thu Apr 24 23:12:40 EDT 2025 Tue Jul 01 02:41:14 EDT 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 4 |
| Language | English |
| License | This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c474t-1e44d68f2fc46bd8d6042c198ed98c90df534e2719ede7fa910a2bdf18314f833 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Conceived and designed the experiments: TM PH AD PS. Performed the experiments: TM PH KG. Analyzed the data: TM PH AD PS. Contributed reagents/materials/analysis tools: TM PH AD PS. Wrote the paper: TM PH PS. The authors have declared that no competing interests exist. |
| OpenAccessLink | http://journals.scholarsportal.info/openUrl.xqy?doi=10.1371/journal.ppat.1004782 |
| PMID | 25849543 |
| PQID | 1672091059 |
| PQPubID | 23479 |
| ParticipantIDs | doaj_primary_oai_doaj_org_article_658ca7961114403d82191c2cf1809045 pubmedcentral_primary_oai_pubmedcentral_nih_gov_4388470 proquest_miscellaneous_1672091059 pubmed_primary_25849543 crossref_citationtrail_10_1371_journal_ppat_1004782 crossref_primary_10_1371_journal_ppat_1004782 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 2015-04-01 |
| PublicationDateYYYYMMDD | 2015-04-01 |
| PublicationDate_xml | – month: 04 year: 2015 text: 2015-04-01 day: 01 |
| PublicationDecade | 2010 |
| PublicationPlace | United States |
| PublicationPlace_xml | – name: United States – name: San Francisco, CA USA |
| PublicationTitle | PLoS pathogens |
| PublicationTitleAlternate | PLoS Pathog |
| PublicationYear | 2015 |
| Publisher | Public Library of Science Public Library of Science (PLoS) |
| Publisher_xml | – name: Public Library of Science – name: Public Library of Science (PLoS) |
| References | MA Horisberger (ref67) 1987; 68 CD Krause (ref5) 2005; 106 F Flohr (ref68) 1999; 463 O Haller (ref2) 2006; 344 U Muller (ref4) 1994; 264 M Mordstein (ref14) 2010; 84 E de Carvalho (ref58) 2007; 83 J Angel (ref18) 1999; 19 M Mordstein (ref16) 2008; 4 P Hermant (ref44) 2014; 6 I Ioannidis (ref48) 2013; 87 J Wang (ref49) 2009; 182 C Johansson (ref17) 2007; 204 EM Coccia (ref46) 2004; 34 RE Randall (ref1) 2008; 89 MF van den Broek (ref3) 1995; 148 S Crotta (ref27) 2013; 9 ES Barton (ref40) 2003; 111 GA Wilson (ref42) 1994; 68 SV Kotenko (ref11) 2003; 4 G Holloway (ref19) 2013; 94 ref45 PA Phillips (ref61) 1969; 1 T Kawai (ref29) 2006; 7 C Odendall (ref57) 2014; 15 J Pott (ref37) 2012; 8 K Onoguchi (ref56) 2007; 282 C Sommereyns (ref13) 2008; 4 M Derrien (ref41) 2003; 305 M Colonna (ref30) 2002; 14 HM Amerongen (ref36) 1994; 68 SL Sanos (ref69) 2010; 612 JR Fulton (ref31) 2004; 39 G Trinchieri (ref63) 2010; 207 AS Major (ref33) 1998; 233 J Pott (ref23) 2011; 108 C Schindler (ref7) 2007; 282 E Thomas (ref55) 2012; 142 AN Theofilopoulos (ref6) 2005; 23 MC Abt (ref26) 2012; 37 Z Makowska (ref66) 2011; 53 M Mordstein (ref15) 2010; 30 CJ Clarke (ref9) 2001; 1 KR Dionne (ref34) 2011; 17 P Sheppard (ref12) 2003; 4 M Riepenhoff-Talty (ref62) 1993; 33 T Okabayashi (ref52) 2011; 160 S Marukian (ref54) 2011; 54 MR Khaitov (ref51) 2009; 64 KL Tyler (ref60) 1998; 27 JW Schoggins (ref10) 2011; 472 GR Stark (ref8) 2012; 36 MA Mann (ref39) 2002; 303 S Davidson (ref64) 2014; 5 N Feng (ref21) 2008; 82 SC Ganal (ref25) 2012; 37 A Boasso (ref65) 2008; 3 JR Teijaro (ref20) 2013; 340 S Ohka (ref22) 2007; 81 A Sen (ref28) 2012; 109 N Ank (ref47) 2008; 180 MM Arnold (ref38) 2013; 9 T Taniguchi (ref24) 2001; 2 KL Tyler (ref43) 2010; 16 DH Rubin (ref35) 1986; 1 S Zahn (ref53) 2011; 131 R Morecki (ref59) 1982; 307 NA Jewell (ref50) 2010; 84 D Chen (ref32) 2001; 23 |
| References_xml | – volume: 37 start-page: 171 year: 2012 ident: ref25 article-title: Priming of natural killer cells by nonmucosal mononuclear phagocytes requires instructive signals from commensal microbiota publication-title: Immunity doi: 10.1016/j.immuni.2012.05.020 – volume: 39 start-page: 1285 year: 2004 ident: ref31 article-title: Mucosal and systemic immunity to intestinal reovirus infection in aged mice publication-title: Exp Gerontol doi: 10.1016/j.exger.2004.06.013 – volume: 30 start-page: 579 year: 2010 ident: ref15 article-title: What have we learned from the IL28 receptor knockout mouse? publication-title: J Interferon Cytokine Res doi: 10.1089/jir.2010.0061 – volume: 131 start-page: 133 year: 2011 ident: ref53 article-title: Evidence for a pathophysiological role of keratinocyte-derived type III interferon (IFNlambda) in cutaneous lupus erythematosus publication-title: J Invest Dermatol doi: 10.1038/jid.2010.244 – volume: 340 start-page: 207 year: 2013 ident: ref20 article-title: Persistent LCMV infection is controlled by blockade of type I interferon signaling publication-title: Science doi: 10.1126/science.1235214 – volume: 53 start-page: 1154 year: 2011 ident: ref66 article-title: Interferon-beta and interferon-lambda signaling is not affected by interferon-induced refractoriness to interferon-alpha in vivo publication-title: Hepatology doi: 10.1002/hep.24189 – volume: 4 start-page: e1000151 year: 2008 ident: ref16 article-title: Interferon-lambda contributes to innate immunity of mice against influenza A virus but not against hepatotropic viruses publication-title: PLoS Pathog doi: 10.1371/journal.ppat.1000151 – volume: 142 start-page: 978 year: 2012 ident: ref55 article-title: HCV infection induces a unique hepatic innate immune response associated with robust production of type III interferons publication-title: Gastroenterology doi: 10.1053/j.gastro.2011.12.055 – volume: 111 start-page: 1823 year: 2003 ident: ref40 article-title: Utilization of sialic acid as a coreceptor is required for reovirus-induced biliary disease publication-title: J Clin Invest doi: 10.1172/JCI16303 – volume: 37 start-page: 158 year: 2012 ident: ref26 article-title: Commensal bacteria calibrate the activation threshold of innate antiviral immunity publication-title: Immunity doi: 10.1016/j.immuni.2012.04.011 – volume: 282 start-page: 7576 year: 2007 ident: ref56 article-title: Viral infections activate types I and III interferon genes through a common mechanism publication-title: J Biol Chem doi: 10.1074/jbc.M608618200 – volume: 17 start-page: 314 year: 2011 ident: ref34 article-title: Type I interferon signaling limits reoviral tropism within the brain and prevents lethal systemic infection publication-title: J Neurovirol doi: 10.1007/s13365-011-0038-1 – volume: 108 start-page: 7944 year: 2011 ident: ref23 article-title: IFN-lambda determines the intestinal epithelial antiviral host defense publication-title: Proc Natl Acad Sci U S A doi: 10.1073/pnas.1100552108 – volume: 33 start-page: 394 year: 1993 ident: ref62 article-title: Group A rotaviruses produce extrahepatic biliary obstruction in orally inoculated newborn mice publication-title: Pediatr Res – volume: 64 start-page: 375 year: 2009 ident: ref51 article-title: Respiratory virus induction of alpha-, beta- and lambda-interferons in bronchial epithelial cells and peripheral blood mononuclear cells publication-title: Allergy doi: 10.1111/j.1398-9995.2008.01826.x – volume: 233 start-page: 163 year: 1998 ident: ref33 article-title: Mucosal immunity to reovirus infection publication-title: Curr Top Microbiol Immunol – volume: 84 start-page: 5670 year: 2010 ident: ref14 article-title: Lambda interferon renders epithelial cells of the respiratory and gastrointestinal tracts resistant to viral infections publication-title: J Virol doi: 10.1128/JVI.00272-10 – volume: 109 start-page: 20667 year: 2012 ident: ref28 article-title: Innate immune response to homologous rotavirus infection in the small intestinal villous epithelium at single-cell resolution publication-title: Proc Natl Acad Sci U S A doi: 10.1073/pnas.1212188109 – volume: 307 start-page: 481 year: 1982 ident: ref59 article-title: Biliary atresia and reovirus type 3 infection publication-title: N Engl J Med doi: 10.1056/NEJM198208193070806 – volume: 82 start-page: 7578 year: 2008 ident: ref21 article-title: Role of interferon in homologous and heterologous rotavirus infection in the intestines and extraintestinal organs of suckling mice publication-title: J Virol doi: 10.1128/JVI.00391-08 – volume: 36 start-page: 503 year: 2012 ident: ref8 article-title: The JAK-STAT pathway at twenty publication-title: Immunity doi: 10.1016/j.immuni.2012.03.013 – volume: 160 start-page: 360 year: 2011 ident: ref52 article-title: Type-III interferon, not type-I, is the predominant interferon induced by respiratory viruses in nasal epithelial cells publication-title: Virus Res doi: 10.1016/j.virusres.2011.07.011 – volume: 83 start-page: 105 year: 2007 ident: ref58 article-title: Extrahepatic biliary atresia: current concepts and future directions publication-title: J Pediatr (Rio J) doi: 10.2223/JPED.1608 – volume: 89 start-page: 1 year: 2008 ident: ref1 article-title: Interferons and viruses: an interplay between induction, signalling, antiviral responses and virus countermeasures publication-title: J Gen Virol doi: 10.1099/vir.0.83391-0 – volume: 68 start-page: 945 issue: Pt 3 year: 1987 ident: ref67 article-title: A recombinant human interferon-alpha B/D hybrid with a broad host-range publication-title: J Gen Virol doi: 10.1099/0022-1317-68-3-945 – volume: 207 start-page: 2053 year: 2010 ident: ref63 article-title: Type I interferon: friend or foe? publication-title: J Exp Med doi: 10.1084/jem.20101664 – volume: 1 start-page: 117 year: 2001 ident: ref9 article-title: Mechanisms of interferon mediated anti-viral resistance publication-title: Curr Drug Targets Immune Endocr Metabol Disord doi: 10.2174/1568005310101020117 – volume: 305 start-page: 25 year: 2003 ident: ref41 article-title: The M2 gene segment is involved in the capacity of reovirus type 3Abney to induce the oily fur syndrome in neonatal mice, a S1 gene segment-associated phenotype publication-title: Virology doi: 10.1006/viro.2002.1723 – volume: 14 start-page: 373 year: 2002 ident: ref30 article-title: Interferon-producing cells: on the front line in immune responses against pathogens publication-title: Curr Opin Immunol doi: 10.1016/S0952-7915(02)00349-7 – volume: 23 start-page: 229 year: 2001 ident: ref32 article-title: Mucosal T cell response to reovirus publication-title: Immunol Res doi: 10.1385/IR:23:2-3:229 – volume: 4 start-page: 63 year: 2003 ident: ref12 article-title: IL-28, IL-29 and their class II cytokine receptor IL-28R publication-title: Nat Immunol doi: 10.1038/ni873 – ident: ref45 doi: 10.1126/science.1258100 – volume: 4 start-page: e1000017 year: 2008 ident: ref13 article-title: IFN-lambda (IFN-lambda) is expressed in a tissue-dependent fashion and primarily acts on epithelial cells in vivo publication-title: PLoS Pathog doi: 10.1371/journal.ppat.1000017 – volume: 19 start-page: 655 year: 1999 ident: ref18 article-title: Lack of a role for type I and type II interferons in the resolution of rotavirus-induced diarrhea and infection in mice publication-title: J Interferon Cytokine Res doi: 10.1089/107999099313802 – volume: 54 start-page: 1913 year: 2011 ident: ref54 article-title: Hepatitis C virus induces interferon-lambda and interferon-stimulated genes in primary liver cultures publication-title: Hepatology doi: 10.1002/hep.24580 – volume: 34 start-page: 796 year: 2004 ident: ref46 article-title: Viral infection and Toll-like receptor agonists induce a differential expression of type I and lambda interferons in human plasmacytoid and monocyte-derived dendritic cells publication-title: Eur J Immunol doi: 10.1002/eji.200324610 – volume: 344 start-page: 119 year: 2006 ident: ref2 article-title: The interferon response circuit: induction and suppression by pathogenic viruses publication-title: Virology doi: 10.1016/j.virol.2005.09.024 – volume: 9 start-page: e1003064 year: 2013 ident: ref38 article-title: The battle between rotavirus and its host for control of the interferon signaling pathway publication-title: PLoS Pathog doi: 10.1371/journal.ppat.1003064 – volume: 16 start-page: 56 year: 2010 ident: ref43 article-title: Gene expression in the brain during reovirus encephalitis publication-title: J Neurovirol doi: 10.3109/13550280903586394 – volume: 148 start-page: 5 year: 1995 ident: ref3 article-title: Immune defence in mice lacking type I and/or type II interferon receptors publication-title: Immunol Rev doi: 10.1111/j.1600-065X.1995.tb00090.x – volume: 7 start-page: 131 year: 2006 ident: ref29 article-title: Innate immune recognition of viral infection publication-title: Nat Immunol doi: 10.1038/ni1303 – volume: 27 start-page: 1475 year: 1998 ident: ref60 article-title: Detection of reovirus RNA in hepatobiliary tissues from patients with extrahepatic biliary atresia and choledochal cysts publication-title: Hepatology doi: 10.1002/hep.510270603 – volume: 68 start-page: 6458 year: 1994 ident: ref42 article-title: Association of the reovirus S1 gene with serotype 3-induced biliary atresia in mice publication-title: J Virol doi: 10.1128/JVI.68.10.6458-6465.1994 – volume: 4 start-page: 69 year: 2003 ident: ref11 article-title: IFN-lambdas mediate antiviral protection through a distinct class II cytokine receptor complex publication-title: Nat Immunol doi: 10.1038/ni875 – volume: 8 start-page: e1002670 year: 2012 ident: ref37 article-title: Age-dependent TLR3 expression of the intestinal epithelium contributes to rotavirus susceptibility publication-title: PLoS Pathog doi: 10.1371/journal.ppat.1002670 – volume: 303 start-page: 222 year: 2002 ident: ref39 article-title: Type 3 reovirus neuroinvasion after intramuscular inoculation: direct invasion of nerve terminals and age-dependent pathogenesis publication-title: Virology doi: 10.1006/viro.2002.1699 – volume: 94 start-page: 1151 year: 2013 ident: ref19 article-title: Innate cellular responses to rotavirus infection publication-title: J Gen Virol doi: 10.1099/vir.0.051276-0 – volume: 9 start-page: e1003773 year: 2013 ident: ref27 article-title: Type I and type III interferons drive redundant amplification loops to induce a transcriptional signature in influenza-infected airway epithelia publication-title: PLoS Pathog doi: 10.1371/journal.ppat.1003773 – volume: 180 start-page: 2474 year: 2008 ident: ref47 article-title: An important role for type III interferon (IFN-lambda/IL-28) in TLR-induced antiviral activity publication-title: J Immunol doi: 10.4049/jimmunol.180.4.2474 – volume: 87 start-page: 3261 year: 2013 ident: ref48 article-title: Toll-like receptor expression and induction of type I and type III interferons in primary airway epithelial cells publication-title: J Virol doi: 10.1128/JVI.01956-12 – volume: 282 start-page: 20059 year: 2007 ident: ref7 article-title: JAK-STAT signaling: from interferons to cytokines publication-title: J Biol Chem doi: 10.1074/jbc.R700016200 – volume: 15 start-page: 717 year: 2014 ident: ref57 article-title: Diverse intracellular pathogens activate type III interferon expression from peroxisomes publication-title: Nat Immunol doi: 10.1038/ni.2915 – volume: 81 start-page: 7902 year: 2007 ident: ref22 article-title: Establishment of a poliovirus oral infection system in human poliovirus receptor-expressing transgenic mice that are deficient in alpha/beta interferon receptor publication-title: J Virol doi: 10.1128/JVI.02675-06 – volume: 472 start-page: 481 year: 2011 ident: ref10 article-title: A diverse range of gene products are effectors of the type I interferon antiviral response publication-title: Nature doi: 10.1038/nature09907 – volume: 106 start-page: 299 year: 2005 ident: ref5 article-title: Evolution of the Class 2 cytokines and receptors, and discovery of new friends and relatives publication-title: Pharmacol Ther doi: 10.1016/j.pharmthera.2004.12.002 – volume: 204 start-page: 1349 year: 2007 ident: ref17 article-title: Type I interferons produced by hematopoietic cells protect mice against lethal infection by mammalian reovirus publication-title: J Exp Med doi: 10.1084/jem.20061587 – volume: 612 start-page: 505 year: 2010 ident: ref69 article-title: Isolation of NK cells and NK-like cells from the intestinal lamina propria publication-title: Methods Mol Biol doi: 10.1007/978-1-60761-362-6_32 – volume: 84 start-page: 11515 year: 2010 ident: ref50 article-title: Lambda interferon is the predominant interferon induced by influenza A virus infection in vivo publication-title: J Virol doi: 10.1128/JVI.01703-09 – volume: 264 start-page: 1918 year: 1994 ident: ref4 article-title: Functional role of type I and type II interferons in antiviral defense publication-title: Science doi: 10.1126/science.8009221 – volume: 5 start-page: 3864 year: 2014 ident: ref64 article-title: Pathogenic potential of interferon alphabeta in acute influenza infection publication-title: Nat Commun doi: 10.1038/ncomms4864 – volume: 6 start-page: 563 year: 2014 ident: ref44 article-title: Interferon-lambda in the context of viral infections: production, response and therapeutic implications publication-title: J Innate Immun doi: 10.1159/000360084 – volume: 2 start-page: 378 year: 2001 ident: ref24 article-title: A weak signal for strong responses: interferon-alpha/beta revisited publication-title: Nat Rev Mol Cell Biol doi: 10.1038/35073080 – volume: 1 start-page: 193 year: 1969 ident: ref61 article-title: Chronic obstructive jaundice induced by Reovirus type 3 in weanling mice publication-title: Pathology doi: 10.3109/00313026909071296 – volume: 1 start-page: 79 year: 1986 ident: ref35 article-title: Reovirus infection in adult mice: the virus hemagglutinin determines the site of intestinal disease publication-title: Microb Pathog doi: 10.1016/0882-4010(86)90034-3 – volume: 23 start-page: 307 year: 2005 ident: ref6 article-title: Type I interferons (alpha/beta) in immunity and autoimmunity publication-title: Annu Rev Immunol doi: 10.1146/annurev.immunol.23.021704.115843 – volume: 3 start-page: e2961 year: 2008 ident: ref65 article-title: HIV-induced type I interferon and tryptophan catabolism drive T cell dysfunction despite phenotypic activation publication-title: PLoS One doi: 10.1371/journal.pone.0002961 – volume: 182 start-page: 1296 year: 2009 ident: ref49 article-title: Differentiated human alveolar type II cells secrete antiviral IL-29 (IFN-lambda 1) in response to influenza A infection publication-title: J Immunol doi: 10.4049/jimmunol.182.3.1296 – volume: 463 start-page: 24 year: 1999 ident: ref68 article-title: The central interactive region of human MxA GTPase is involved in GTPase activation and interaction with viral target structures publication-title: FEBS Lett doi: 10.1016/S0014-5793(99)01598-7 – volume: 68 start-page: 8428 year: 1994 ident: ref36 article-title: Proteolytic processing of reovirus is required for adherence to intestinal M cells publication-title: J Virol doi: 10.1128/JVI.68.12.8428-8432.1994 |
| SSID | ssj0041316 |
| Score | 2.540884 |
| Snippet | Epithelial cells are a major port of entry for many viruses, but the molecular networks which protect barrier surfaces against viral infections are... |
| SourceID | doaj pubmedcentral proquest pubmed crossref |
| SourceType | Open Website Open Access Repository Aggregation Database Index Database Enrichment Source |
| StartPage | e1004782 |
| SubjectTerms | Animals Cell Separation Epithelial Cells - immunology Flow Cytometry Humans Immunohistochemistry Interferon-alpha - immunology Interferon-beta - immunology Interferon-gamma - immunology Intestinal Mucosa - immunology Leukocytes - immunology Mammalian orthoreovirus 3 - immunology Mice Mice, Knockout Polymerase Chain Reaction Reoviridae Infections - immunology |
| SummonAdditionalLinks | – databaseName: DOAJ Directory of Open Access Journals dbid: DOA link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV3NatwwEBYlUOil9L_uHyr0qu7KmpXkY1u6pKXNqYHcjCyNyNLUu2S9gfQl8izpte-QZ-rIspdsKeTSm7ElLDTfjD6h0TeMvQmmaVRjpUBlUYDRIFyUIAxG4nPgdZTpgvPXA71_CJ-PZkfXSn2lnLAsD5wnbkIrpHem0uSTAFMVLLmY9KWPSXiK-EiKvrTmjZupHIMpMvdFT1NRHGGU1sOlOWXkZLDR29XKJfnopE5T7ixKvXb_vwjn33mT1xai-T12d2CQ_F0e-X12C9sH7HauKXn-kF18wc33pT_vUARC1xkG_ml-IK4uJ1e_uGsDx1W6hnFCuMsffnO_HDMGuOM5Kb3Lmv-Ln9T9R0pqp9YBI-15kWfxZ94du46nyh4USbs1T9qe9MTPFqebNR9zvNr1I3Y4__jtw74Yqi4IDwY6IREgaBvL6EE3wQZNfu1lZTFU1lfTEGcKsDSywoAmOuIbrmwC2UNJiFapx2yvXbb4lPEyEJ-pPOEhABhVNhFpPxmdI6KAZqoLpsZpr_0gSZ4qY5zU_Tmboa1JntM6GasejFUwse21ypIcN7R_nyy6bZsEtfsXBLN6gFl9E8wK9nrEQ00OmE5VXIvLzbqW2iQAEk0t2JOMj-2vSqJ31QxUwcwOcnbGsvulXRz3It-gLBGH6bP_Mfjn7A7xvFlOOHrB9rrTDb4kLtU1r3q3-QNfiyEK priority: 102 providerName: Directory of Open Access Journals |
| Title | Leukocyte-Derived IFN-α/β and Epithelial IFN-λ Constitute a Compartmentalized Mucosal Defense System that Restricts Enteric Virus Infections |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/25849543 https://www.proquest.com/docview/1672091059 https://pubmed.ncbi.nlm.nih.gov/PMC4388470 https://doaj.org/article/658ca7961114403d82191c2cf1809045 |
| Volume | 11 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV3LjtMwFLWGGSGxQbwJj8pIbD00sWMnC4QYptUMohUaUdRd5PjBVFRpSVJE-Qm-Bbb8w3wT13ZaUTQIiW1iJ5F9H8fx9TkIPdWiLGmZxcTQzBAmOCPSxowIYwHPMcVt7A44j8b8ZMJeT9PpHtpotnYD2Fy6tHN6UpN6fvjl0_oFOPxzr9og4k2nw-VSOkJoxzcDQfkAcpNwrjpi230FiNheDNWJ5RBBOe8O0_3tKY4qGDJ0njK6k7c8vf9lmPTP0srfctXwBrregUz8MljFTbRnqlvoapCdXN9G396Y1ceFWreGHIMBfjYanw7H5OL7s4sfWFYaD5bupMYcTDPc-ImdrmcoKsAS-xhSt0EWYPYVuo9c3Tu0PjYWlsUGBx503J7LFp8ZJw2i2gb7AoSZwu9n9arBp10ZWNXcQZPh4N2rE9IJMxDFBGtJbBjTPLOJVYyXOtMcXF_FeWZ0nqm8r21KmUlEnBtthJUASWRSagvhI2Y2o_Qu2q8WlbmPcKIB8uQKTEYzJmhSWgNLTislYAkj-jxCdDPshepYy514xrzwW3ECVi9hTAs3b0U3bxEi217LwNrxj_ZHbka3bR3ntr-wqD8UnQsXgNWUFDmH7MBYn-oMgn2sEmUdBRog4wg92dhDAT7qNl5kZRarpoi5SBwuS_MI3Qv2sX3Vxr4iJHYsZ-dbdu9Us3PPA85oBtii_-C_ez5E1wD_paEQ6RHab-uVeQwYqy176IqYih46OBqM3571_J-KnnelX6MhMAE |
| linkProvider | Scholars Portal |
| 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=Leukocyte-Derived+IFN-%CE%B1%2F%CE%B2+and+Epithelial+IFN-%CE%BB+Constitute+a+Compartmentalized+Mucosal+Defense+System+that+Restricts+Enteric+Virus+Infections&rft.jtitle=PLoS+pathogens&rft.au=Mahlak%C3%B5iv%2C+Tanel&rft.au=Hernandez%2C+Pedro&rft.au=Gronke%2C+Konrad&rft.au=Diefenbach%2C+Andreas&rft.date=2015-04-01&rft.pub=Public+Library+of+Science&rft.issn=1553-7366&rft.eissn=1553-7374&rft.volume=11&rft.issue=4&rft_id=info:doi/10.1371%2Fjournal.ppat.1004782&rft_id=info%3Apmid%2F25849543&rft.externalDocID=PMC4388470 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1553-7374&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1553-7374&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1553-7374&client=summon |