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Article: Deficiency of the B cell-activating factor receptor results in limited CD169+ macrophage function during viral infection

TitleDeficiency of the B cell-activating factor receptor results in limited CD169<sup>+</sup> macrophage function during viral infection
Authors
Issue Date2015
Citation
Journal of Virology, 2015, v. 89, n. 9, p. 4748-4759 How to Cite?
Abstract© 2015, American Society for Microbiology. The B cell-activating factor (BAFF) is critical for B cell development and humoral immunity in mice and humans. While the role of BAFF in B cells has been widely described, its role in innate immunity remains unknown. Using BAFF receptor (BAFFR)-deficient mice, we characterized BAFFR-related innate and adaptive immune functions following infection with vesicular stomatitis virus (VSV) and lymphocytic choriomeningitis virus (LCMV).Weidentified a critical role for BAFFR signaling in the generation and maintenance of the CD169+ macrophage compartment. Consequently, Baffr-/- mice exhibited limited induction of innate type I interferon production after viral infection. Lack of BAFFR signaling reduced virus amplification and presentation following viral infection, resulting in highly reduced antiviral adaptive immune responses. As a consequence, BAFFR-deficient mice showed exacerbated and fatal disease after viral infection. Mechanistically, transient lack of B cells in Baffr-/- animals resulted in limited lymphotoxin expression, which is critical for maintenance of CD169+ cells. In conclusion, BAFFR signaling affects both innate and adaptive immune activation during viral infections.
Persistent Identifierhttp://hdl.handle.net/10722/292881
ISSN
2023 Impact Factor: 4.0
2023 SCImago Journal Rankings: 1.378
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorXu, Haifeng C.-
dc.contributor.authorHuang, Jun-
dc.contributor.authorKhairnar, Vishal-
dc.contributor.authorDuhan, Vikas-
dc.contributor.authorPandyra, Aleksandra A.-
dc.contributor.authorGrusdat, Melanie-
dc.contributor.authorShinde, Prashant-
dc.contributor.authorMcIlwain, David R.-
dc.contributor.authorManey, Sathish Kumar-
dc.contributor.authorGommerman, Jennifer-
dc.contributor.authorLöhning, Max-
dc.contributor.authorOhashi, Pamela S.-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorPieper, Kathrin-
dc.contributor.authorSic, Heiko-
dc.contributor.authorSpeletas, Matthaios-
dc.contributor.authorEibel, Hermann-
dc.contributor.authorWare, Carl F.-
dc.contributor.authorTumanov, Alexei V.-
dc.contributor.authorKruglov, Andrey A.-
dc.contributor.authorNedospasov, Sergei A.-
dc.contributor.authorHäusinger, Dieter-
dc.contributor.authorRecher, Mike-
dc.contributor.authorLang, Karl S.-
dc.contributor.authorLang, Philipp A.-
dc.date.accessioned2020-11-17T14:57:24Z-
dc.date.available2020-11-17T14:57:24Z-
dc.date.issued2015-
dc.identifier.citationJournal of Virology, 2015, v. 89, n. 9, p. 4748-4759-
dc.identifier.issn0022-538X-
dc.identifier.urihttp://hdl.handle.net/10722/292881-
dc.description.abstract© 2015, American Society for Microbiology. The B cell-activating factor (BAFF) is critical for B cell development and humoral immunity in mice and humans. While the role of BAFF in B cells has been widely described, its role in innate immunity remains unknown. Using BAFF receptor (BAFFR)-deficient mice, we characterized BAFFR-related innate and adaptive immune functions following infection with vesicular stomatitis virus (VSV) and lymphocytic choriomeningitis virus (LCMV).Weidentified a critical role for BAFFR signaling in the generation and maintenance of the CD169+ macrophage compartment. Consequently, Baffr-/- mice exhibited limited induction of innate type I interferon production after viral infection. Lack of BAFFR signaling reduced virus amplification and presentation following viral infection, resulting in highly reduced antiviral adaptive immune responses. As a consequence, BAFFR-deficient mice showed exacerbated and fatal disease after viral infection. Mechanistically, transient lack of B cells in Baffr-/- animals resulted in limited lymphotoxin expression, which is critical for maintenance of CD169+ cells. In conclusion, BAFFR signaling affects both innate and adaptive immune activation during viral infections.-
dc.languageeng-
dc.relation.ispartofJournal of Virology-
dc.titleDeficiency of the B cell-activating factor receptor results in limited CD169<sup>+</sup> macrophage function during viral infection-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1128/JVI.02976-14-
dc.identifier.pmid25673724-
dc.identifier.pmcidPMC4403498-
dc.identifier.scopuseid_2-s2.0-84928567018-
dc.identifier.volume89-
dc.identifier.issue9-
dc.identifier.spage4748-
dc.identifier.epage4759-
dc.identifier.eissn1098-5514-
dc.identifier.isiWOS:000352219600005-
dc.identifier.issnl0022-538X-

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