Article: A critical role of IL-17 in modulating the B-cell response during H5N1 influenza virus infection

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TitleA critical role of IL-17 in modulating the B-cell response during H5N1 influenza virus infection
AuthorsWang, X1
Chan, CCS1
Yang, M1
Deng, J1
Poon, VKM1
Leung, VHC1
Ko, KH1
Zhou, J1
Yung Yuen, K1
Zheng, BJ1
Lu, L1
KeywordsB cell
H5N1 influenza virus
IL-17
lung infection
Issue Date2011
PublisherChinese Society of Immunology. The Journal's web site is located at http://www.nature.com/cmi/index.html
CitationCellular And Molecular Immunology, 2011, v. 8 n. 6, p. 462-468 [How to Cite?]
DOI: http://dx.doi.org/10.1038/cmi.2011.38
AbstractInterleukin-17 (IL-17), a member of the IL-17 cytokine family, plays a crucial role in mediating the immune response against extracellular bacteria and fungi in the lung. Although there is increasing evidence that IL-17 is involved in protective immunity against H1 and H3 influenza virus infections, little is known about the role of IL-17 in the highly pathogenic H5N1 influenza virus infection. In this study, we show that H5N1-infected IL-17 knockout (KO) mice exhibit markedly increased weight loss, more pronounced lung immunopathology and significantly reduced survival rates as compared with infected wild-type controls. Moreover, the frequency of B cells in the lung were substantially decreased in IL-17 KO mice after virus infection, which correlated with reduced CXCR5 expression in B cells and decreased CXCL13 production in the lung tissue of IL-17 KO mice. Consistent with this observation, B cells from IL-17 KO mice exhibited a significant reduction in chemokine-mediated migration in culture. Taken together, these findings demonstrate a critical role for IL-17 in mediating the recruitment of B cells to the site of pulmonary influenza virus infection in mice. © 2011 CSI and USTC. All rights reserved.
ISSN1672-7681
2011 Impact Factor: 2.992
2011 SCImago Journal Rankings: 0.341
DOIhttp://dx.doi.org/10.1038/cmi.2011.38
ReferencesReferences in Scopus
GrantsThe role of IL-17 in modulating B cell functions duringin anti-viral immunity against H5N1 influenza infection in mice
DC Field
Value
dc.contributor.authorWang, X
dc.contributor.authorChan, CCS
dc.contributor.authorYang, M
dc.contributor.authorDeng, J
dc.contributor.authorPoon, VKM
dc.contributor.authorLeung, VHC
dc.contributor.authorKo, KH
dc.contributor.authorZhou, J
dc.contributor.authorYung Yuen, K
dc.contributor.authorZheng, BJ
dc.contributor.authorLu, L
dc.date.accessioned2012-05-29T06:14:24Z
dc.date.available2012-05-29T06:14:24Z
dc.date.issued2011
dc.description.abstractInterleukin-17 (IL-17), a member of the IL-17 cytokine family, plays a crucial role in mediating the immune response against extracellular bacteria and fungi in the lung. Although there is increasing evidence that IL-17 is involved in protective immunity against H1 and H3 influenza virus infections, little is known about the role of IL-17 in the highly pathogenic H5N1 influenza virus infection. In this study, we show that H5N1-infected IL-17 knockout (KO) mice exhibit markedly increased weight loss, more pronounced lung immunopathology and significantly reduced survival rates as compared with infected wild-type controls. Moreover, the frequency of B cells in the lung were substantially decreased in IL-17 KO mice after virus infection, which correlated with reduced CXCR5 expression in B cells and decreased CXCL13 production in the lung tissue of IL-17 KO mice. Consistent with this observation, B cells from IL-17 KO mice exhibited a significant reduction in chemokine-mediated migration in culture. Taken together, these findings demonstrate a critical role for IL-17 in mediating the recruitment of B cells to the site of pulmonary influenza virus infection in mice. © 2011 CSI and USTC. All rights reserved.
dc.description.grantThe role of IL-17 in modulating B cell functions duringin anti-viral immunity against H5N1 influenza infection in mice
dc.description.grantcode103752
dc.description.natureLink_to_subscribed_fulltext
dc.identifier.citationCellular And Molecular Immunology, 2011, v. 8 n. 6, p. 462-468 [How to Cite?]
DOI: http://dx.doi.org/10.1038/cmi.2011.38
dc.identifier.doihttp://dx.doi.org/10.1038/cmi.2011.38
dc.identifier.epage468
dc.identifier.hkuros208186
dc.identifier.isiWOS:000296758700005
Funding AgencyGrant Number
Food and Health Bureau, Hong Kong SAR Government10091002
Funding Information:

We are grateful to Dr Yoichiro Iwakura (The University of Tokyo) for providing IL-17 KO mice. This work was supported by the Research Fund for the Control of Infectious Diseases (RFCID), Food and Health Bureau, Hong Kong SAR Government (No. 10091002). The authors declare no financial or commercial conflicts of interest.

dc.identifier.issn1672-7681
2011 Impact Factor: 2.992
2011 SCImago Journal Rankings: 0.341
dc.identifier.issue6
dc.identifier.pmid21946434
dc.identifier.scopuseid_2-s2.0-80055117444
dc.identifier.spage462
dc.identifier.urihttp://hdl.handle.net/10722/148655
dc.identifier.volume8
dc.languageeng
dc.publisherChinese Society of Immunology. The Journal's web site is located at http://www.nature.com/cmi/index.html
dc.publisher.placeChina
dc.relation.ispartofCellular and Molecular Immunology
dc.relation.referencesReferences in Scopus
dc.subject.meshAnimals
dc.subject.meshB-Lymphocytes - Cytology - Immunology - Metabolism
dc.subject.meshCell Movement - Immunology
dc.subject.meshChemokine Cxcl13 - Biosynthesis - Immunology
dc.subject.meshDown-Regulation
dc.subject.meshFemale
dc.subject.meshFlow Cytometry
dc.subject.meshGene Deletion
dc.subject.meshHumans
dc.subject.meshInfluenza A Virus, H5n1 Subtype - Immunology - Pathogenicity
dc.subject.meshInfluenza, Human - Immunology - Pathology - Virology
dc.subject.meshInterleukin-17 - Deficiency - Genetics - Immunology
dc.subject.meshLung - Immunology - Pathology - Virology
dc.subject.meshMale
dc.subject.meshMice
dc.subject.meshMice, Inbred C57bl
dc.subject.meshMice, Knockout
dc.subject.meshOrthomyxoviridae Infections - Immunology - Mortality - Pathology - Virology
dc.subject.meshReceptors, Cxcr5 - Biosynthesis - Immunology
dc.subject.meshSurvival Rate
dc.subject.meshWeight Loss
dc.subjectB cell
dc.subjectH5N1 influenza virus
dc.subjectIL-17
dc.subjectlung infection
dc.titleA critical role of IL-17 in modulating the B-cell response during H5N1 influenza virus infection
dc.typeArticle
Author Affiliations
  1. The University of Hong Kong