title: A critical role of IL-17 in modulating the B-cell response during H5N1 influenza virus infection.
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.
authors.affiliation: Department of Pathology, The University of Hong Kong, Hong Kong, China.
authors.forename: Xiaohui
authors.initials: X
authors.lastname: Wang
authors.forename: Chris C S
authors.initials: CC
authors.lastname: Chan
authors.forename: Min
authors.initials: M
authors.lastname: Yang
authors.forename: Jun
authors.initials: J
authors.lastname: Deng
authors.forename: Vincent K M
authors.initials: VK
authors.lastname: Poon
authors.forename: Virtual H C
authors.initials: VH
authors.lastname: Leung
authors.forename: King-Hung
authors.initials: KH
authors.lastname: Ko
authors.forename: Jie
authors.initials: J
authors.lastname: Zhou
authors.forename: Kwok Yung
authors.initials: KY
authors.lastname: Yuen
authors.forename: Bo-Jian
authors.initials: BJ
authors.lastname: Zheng
authors.forename: Liwei
authors.initials: L
authors.lastname: Lu
mesh_terms: D000818:Animals; D001402:B-Lymphocytes / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D002465:Cell Movement / Q000276:immunology; D054382:Chemokine CXCL13 / Q000096:biosynthesis / Q000276:immunology; D015536:Down-Regulation; D005260:Female; D005434:Flow Cytometry; D017353:Gene Deletion; D006801:Humans; D053124:Influenza A Virus, H5N1 Subtype / Q000276:immunology* / Q000472:pathogenicity; D007251:Influenza, Human / Q000276:immunology / Q000473:pathology / Q000821:virology; D020381:Interleukin-17 / Q000172:deficiency / Q000235:genetics / Q000276:immunology*; D008168:Lung / Q000276:immunology / Q000473:pathology / Q000821:virology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009976:Orthomyxoviridae Infections / Q000276:immunology* / Q000401:mortality / Q000473:pathology / Q000821:virology; D054380:Receptors, CXCR5 / Q000096:biosynthesis / Q000276:immunology; D015996:Survival Rate; D015431:Weight Loss
chemical_list: C513179:CXCR5 protein, mouse; D054382:Chemokine CXCL13; C486386:Cxcl13 protein, mouse; D020381:Interleukin-17; D054380:Receptors, CXCR5