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- Publisher Website: 10.1038/cmi.2011.38
- Scopus: eid_2-s2.0-80055117444
- PMID: 21946434
- WOS: WOS:000296758700005
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Article: A critical role of IL-17 in modulating the B-cell response during H5N1 influenza virus infection
Title | A critical role of IL-17 in modulating the B-cell response during H5N1 influenza virus infection | ||||
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Authors | |||||
Keywords | B cell H5N1 influenza virus IL-17 lung infection | ||||
Issue Date | 2011 | ||||
Publisher | Chinese Society of Immunology. The Journal's web site is located at http://www.nature.com/cmi/index.html | ||||
Citation | Cellular And Molecular Immunology, 2011, v. 8 n. 6, p. 462-468 How to Cite? | ||||
Abstract | Interleukin-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. | ||||
Persistent Identifier | http://hdl.handle.net/10722/148655 | ||||
ISSN | 2023 Impact Factor: 21.8 2023 SCImago Journal Rankings: 4.838 | ||||
PubMed Central ID | |||||
ISI Accession Number ID |
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. | ||||
References | |||||
Grants |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Wang, X | en_HK |
dc.contributor.author | Chan, CCS | en_HK |
dc.contributor.author | Yang, M | en_HK |
dc.contributor.author | Deng, J | en_HK |
dc.contributor.author | Poon, VKM | en_HK |
dc.contributor.author | Leung, VHC | en_HK |
dc.contributor.author | Ko, KH | en_HK |
dc.contributor.author | Zhou, J | en_HK |
dc.contributor.author | Yuen, KY | en_HK |
dc.contributor.author | Zheng, BJ | en_HK |
dc.contributor.author | Lu, L | en_HK |
dc.date.accessioned | 2012-05-29T06:14:24Z | - |
dc.date.available | 2012-05-29T06:14:24Z | - |
dc.date.issued | 2011 | en_HK |
dc.identifier.citation | Cellular And Molecular Immunology, 2011, v. 8 n. 6, p. 462-468 | en_HK |
dc.identifier.issn | 1672-7681 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/148655 | - |
dc.description.abstract | Interleukin-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. | en_HK |
dc.language | eng | en_US |
dc.publisher | Chinese Society of Immunology. The Journal's web site is located at http://www.nature.com/cmi/index.html | en_HK |
dc.relation.ispartof | Cellular and Molecular Immunology | en_HK |
dc.subject | B cell | en_HK |
dc.subject | H5N1 influenza virus | en_HK |
dc.subject | IL-17 | en_HK |
dc.subject | lung infection | en_HK |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | B-Lymphocytes - Cytology - Immunology - Metabolism | en_US |
dc.subject.mesh | Cell Movement - Immunology | en_US |
dc.subject.mesh | Chemokine Cxcl13 - Biosynthesis - Immunology | en_US |
dc.subject.mesh | Down-Regulation | en_US |
dc.subject.mesh | Female | en_US |
dc.subject.mesh | Flow Cytometry | en_US |
dc.subject.mesh | Gene Deletion | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Influenza A Virus, H5n1 Subtype - Immunology - Pathogenicity | en_US |
dc.subject.mesh | Influenza, Human - Immunology - Pathology - Virology | en_US |
dc.subject.mesh | Interleukin-17 - Deficiency - Genetics - Immunology | en_US |
dc.subject.mesh | Lung - Immunology - Pathology - Virology | en_US |
dc.subject.mesh | Male | en_US |
dc.subject.mesh | Mice | en_US |
dc.subject.mesh | Mice, Inbred C57bl | en_US |
dc.subject.mesh | Mice, Knockout | en_US |
dc.subject.mesh | Orthomyxoviridae Infections - Immunology - Mortality - Pathology - Virology | en_US |
dc.subject.mesh | Receptors, Cxcr5 - Biosynthesis - Immunology | en_US |
dc.subject.mesh | Survival Rate | en_US |
dc.subject.mesh | Weight Loss | en_US |
dc.title | A critical role of IL-17 in modulating the B-cell response during H5N1 influenza virus infection | en_HK |
dc.type | Article | en_HK |
dc.identifier.email | Zhou, J:jiezhou@hku.hk | en_HK |
dc.identifier.email | Yung Yuen, K:kyyuen@hkucc.hku.hk | en_HK |
dc.identifier.email | Zheng, BJ:bzheng@hkucc.hku.hk | en_HK |
dc.identifier.email | Lu, L:liweilu@hkucc.hku.hk | en_HK |
dc.identifier.authority | Zhou, J=rp01412 | en_HK |
dc.identifier.authority | Yung Yuen, K=rp00366 | en_HK |
dc.identifier.authority | Zheng, BJ=rp00353 | en_HK |
dc.identifier.authority | Lu, L=rp00477 | en_HK |
dc.description.nature | link_to_OA_fulltext | en_US |
dc.identifier.doi | 10.1038/cmi.2011.38 | en_HK |
dc.identifier.pmid | 21946434 | - |
dc.identifier.pmcid | PMC4012931 | - |
dc.identifier.scopus | eid_2-s2.0-80055117444 | en_HK |
dc.identifier.hkuros | 208186 | - |
dc.identifier.hkuros | 290607 | - |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-80055117444&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 8 | en_HK |
dc.identifier.issue | 6 | en_HK |
dc.identifier.spage | 462 | en_HK |
dc.identifier.epage | 468 | en_HK |
dc.identifier.isi | WOS:000296758700005 | - |
dc.publisher.place | China | en_HK |
dc.relation.project | The role of IL-17 in modulating B cell functions duringin anti-viral immunity against H5N1 influenza infection in mice | - |
dc.identifier.scopusauthorid | Wang, X=54411517700 | en_HK |
dc.identifier.scopusauthorid | Chan, CCS=16021156900 | en_HK |
dc.identifier.scopusauthorid | Yang, M=35228247800 | en_HK |
dc.identifier.scopusauthorid | Deng, J=54410515000 | en_HK |
dc.identifier.scopusauthorid | Poon, VKM=6603703384 | en_HK |
dc.identifier.scopusauthorid | Leung, VHC=36612082100 | en_HK |
dc.identifier.scopusauthorid | Ko, KH=7202688627 | en_HK |
dc.identifier.scopusauthorid | Zhou, J=7405550443 | en_HK |
dc.identifier.scopusauthorid | Yung Yuen, K=36078079100 | en_HK |
dc.identifier.scopusauthorid | Zheng, BJ=7201780588 | en_HK |
dc.identifier.scopusauthorid | Lu, L=7403963552 | en_HK |
dc.identifier.issnl | 1672-7681 | - |