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dc.creatorXu, H. C.en
dc.creatorHuang, J.en
dc.creatorKhairnar, V.en
dc.creatorDuhan, V.en
dc.creatorPandyra, A. A.en
dc.creatorGrusdat, M.en
dc.creatorShinde, P.en
dc.creatorMcIlwain, D. R.en
dc.creatorManey, S. K.en
dc.creatorGommerman, J.en
dc.creatorLöhning, M.en
dc.creatorOhashi, P. S.en
dc.creatorMak, T. W.en
dc.creatorPieper, K.en
dc.creatorSic, H.en
dc.creatorSpeletas, M.en
dc.creatorEibel, H.en
dc.creatorWare, C. F.en
dc.creatorTumanov, A. V.en
dc.creatorKruglov, A. A.en
dc.creatorNedospasov, S. A.en
dc.creatorHäusinger, D.en
dc.creatorRecher, M.en
dc.creatorLang, K. S.en
dc.creatorLang, P. A.en
dc.date.accessioned2015-11-23T10:54:22Z
dc.date.available2015-11-23T10:54:22Z
dc.date.issued2015
dc.identifier10.1128/JVI.02976-14
dc.identifier.issn0022538X
dc.identifier.urihttp://hdl.handle.net/11615/34721
dc.description.abstractThe 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. © 2015, American Society for Microbiology.en
dc.source.urihttp://www.scopus.com/inward/record.url?eid=2-s2.0-84928567018&partnerID=40&md5=11687e7ff804318e9e6f48ad0cd768ea
dc.subjectB cell activating factor receptoren
dc.subjectinterferonen
dc.subjectlymphotoxinen
dc.subjectmessenger RNAen
dc.subjectrecombinant alpha interferon Aen
dc.subjectsialoadhesinen
dc.subjectadaptive immunityen
dc.subjectanimal cellen
dc.subjectanimal experimenten
dc.subjectanimal modelen
dc.subjectanimal tissueen
dc.subjectantibody titeren
dc.subjectArticleen
dc.subjectB lymphocyteen
dc.subjectcontrolled studyen
dc.subjectdisease exacerbationen
dc.subjectfatalityen
dc.subjectimmunocompetent cellen
dc.subjectinnate immunityen
dc.subjectinterferon productionen
dc.subjectlymphocytic choriomeningitisen
dc.subjectlymphocytopeniaen
dc.subjectmacrophage functionen
dc.subjectmouseen
dc.subjectnonhumanen
dc.subjectpriority journalen
dc.subjectprotein deficiencyen
dc.subjectprotein expressionen
dc.subjectprotein functionen
dc.subjectsignal transductionen
dc.subjectspleenen
dc.subjectvesicular stomatitisen
dc.subjectvirus immunityen
dc.subjectvirus infectionen
dc.subjectvirus replicationen
dc.subjectAnimaliaen
dc.subjectLymphocytic choriomeningitis virusen
dc.subjectMusen
dc.subjectVesicular stomatitis virusen
dc.titleDeficiency of the B cell-activating factor receptor results in limited CD169+ macrophage function during viral infectionen
dc.typejournalArticleen


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