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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 1
Yung Yuen, K1 1
Zheng, BJ1 1
Lu, L1 1
 
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
2012 Impact Factor: 3.419
 
DOIhttp://dx.doi.org/10.1038/cmi.2011.38
 
ISI Accession Number IDWOS: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.

 
ReferencesReferences in Scopus
 
GrantsThe role of IL-17 in modulating B cell functions duringin anti-viral immunity against H5N1 influenza infection in mice
 
DC FieldValue
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.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
2012 Impact Factor: 3.419
 
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.projectThe role of IL-17 in modulating B cell functions duringin anti-viral immunity against H5N1 influenza infection in mice
 
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
 
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Author Affiliations
  1. The University of Hong Kong