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Article: IL-17A Promotes Pulmonary B-1a Cell Differentiation via Induction of Blimp-1 Expression during Influenza Virus Infection

TitleIL-17A Promotes Pulmonary B-1a Cell Differentiation via Induction of Blimp-1 Expression during Influenza Virus Infection
Authors
Issue Date2016
PublisherPublic Library of Science. The Journal's web site is located at http://pathogens.plosjournals.org/perlserv/?request=index-html&issn=1553-7374
Citation
PLoS Pathogens, 2016, v. 12 n. 1, p. e1005367 How to Cite?
AbstractB-1 cells play a critical role in early protection during influenza infections by producing natural IgM antibodies. However, the underlying mechanisms involved in regulating this process are largely unknown. Here we found that during influenza infection pleural cavity B-1a cells rapidly infiltrated lungs, where they underwent plasmacytic differentiation with enhanced IgM production. This process was promoted by IL-17A signaling via induction of Blimp-1 expression and NF-kB activation in B-1a cells. Deficiency of IL-17A led to severely impaired B-1a-derived antibody production in the respiratory tract, resulting in a deficiency in viral clearance. Transfer of B-1a-derived natural antibodies rescued Il17a(-/-) mice from otherwise lethal infections. Together, we identify a critical function of IL-17A in promoting the plasmacytic differentiation of B-1a cells. Our findings provide new insights into the mechanisms underlying the regulation of pulmonary B-1a cell response against influenza infection.
Persistent Identifierhttp://hdl.handle.net/10722/227861
ISSN
2015 Impact Factor: 7.003
2015 SCImago Journal Rankings: 5.185
ISI Accession Number ID
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DC FieldValueLanguage
dc.contributor.authorWang, H-
dc.contributor.authorMa, K-
dc.contributor.authorChen, M-
dc.contributor.authorKo, KH-
dc.contributor.authorZheng, B-
dc.contributor.authorLu, L-
dc.date.accessioned2016-07-21T02:29:13Z-
dc.date.available2016-07-21T02:29:13Z-
dc.date.issued2016-
dc.identifier.citationPLoS Pathogens, 2016, v. 12 n. 1, p. e1005367-
dc.identifier.issn1553-7366-
dc.identifier.urihttp://hdl.handle.net/10722/227861-
dc.description.abstractB-1 cells play a critical role in early protection during influenza infections by producing natural IgM antibodies. However, the underlying mechanisms involved in regulating this process are largely unknown. Here we found that during influenza infection pleural cavity B-1a cells rapidly infiltrated lungs, where they underwent plasmacytic differentiation with enhanced IgM production. This process was promoted by IL-17A signaling via induction of Blimp-1 expression and NF-kB activation in B-1a cells. Deficiency of IL-17A led to severely impaired B-1a-derived antibody production in the respiratory tract, resulting in a deficiency in viral clearance. Transfer of B-1a-derived natural antibodies rescued Il17a(-/-) mice from otherwise lethal infections. Together, we identify a critical function of IL-17A in promoting the plasmacytic differentiation of B-1a cells. Our findings provide new insights into the mechanisms underlying the regulation of pulmonary B-1a cell response against influenza infection.-
dc.languageeng-
dc.publisherPublic Library of Science. The Journal's web site is located at http://pathogens.plosjournals.org/perlserv/?request=index-html&issn=1553-7374-
dc.relation.ispartofPLoS Pathogens-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleIL-17A Promotes Pulmonary B-1a Cell Differentiation via Induction of Blimp-1 Expression during Influenza Virus Infection-
dc.typeArticle-
dc.identifier.emailZheng, B: bzheng@hkucc.hku.hk-
dc.identifier.emailLu, L: liweilu@hkucc.hku.hk-
dc.identifier.authorityZheng, B=rp00353-
dc.identifier.authorityLu, L=rp00477-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.ppat.1005367-
dc.identifier.pmid26735852-
dc.identifier.hkuros264116-
dc.identifier.volume12-
dc.identifier.issue1-
dc.identifier.spagee1005367-
dc.identifier.epagee1005367-
dc.identifier.isiWOS:000369374500023-
dc.publisher.placeUnited States-
dc.relation.projectB-1 cell response and its regulation during influenza virus infection-

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