Deficiency of the B cell-activating factor receptor results in limited CD169+ macrophage function during viral infection
dc.creator | Xu, H. C. | en |
dc.creator | Huang, J. | en |
dc.creator | Khairnar, V. | en |
dc.creator | Duhan, V. | en |
dc.creator | Pandyra, A. A. | en |
dc.creator | Grusdat, M. | en |
dc.creator | Shinde, P. | en |
dc.creator | McIlwain, D. R. | en |
dc.creator | Maney, S. K. | en |
dc.creator | Gommerman, J. | en |
dc.creator | Löhning, M. | en |
dc.creator | Ohashi, P. S. | en |
dc.creator | Mak, T. W. | en |
dc.creator | Pieper, K. | en |
dc.creator | Sic, H. | en |
dc.creator | Speletas, M. | en |
dc.creator | Eibel, H. | en |
dc.creator | Ware, C. F. | en |
dc.creator | Tumanov, A. V. | en |
dc.creator | Kruglov, A. A. | en |
dc.creator | Nedospasov, S. A. | en |
dc.creator | Häusinger, D. | en |
dc.creator | Recher, M. | en |
dc.creator | Lang, K. S. | en |
dc.creator | Lang, P. A. | en |
dc.date.accessioned | 2015-11-23T10:54:22Z | |
dc.date.available | 2015-11-23T10:54:22Z | |
dc.date.issued | 2015 | |
dc.identifier | 10.1128/JVI.02976-14 | |
dc.identifier.issn | 0022538X | |
dc.identifier.uri | http://hdl.handle.net/11615/34721 | |
dc.description.abstract | 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. © 2015, American Society for Microbiology. | en |
dc.source.uri | http://www.scopus.com/inward/record.url?eid=2-s2.0-84928567018&partnerID=40&md5=11687e7ff804318e9e6f48ad0cd768ea | |
dc.subject | B cell activating factor receptor | en |
dc.subject | interferon | en |
dc.subject | lymphotoxin | en |
dc.subject | messenger RNA | en |
dc.subject | recombinant alpha interferon A | en |
dc.subject | sialoadhesin | en |
dc.subject | adaptive immunity | en |
dc.subject | animal cell | en |
dc.subject | animal experiment | en |
dc.subject | animal model | en |
dc.subject | animal tissue | en |
dc.subject | antibody titer | en |
dc.subject | Article | en |
dc.subject | B lymphocyte | en |
dc.subject | controlled study | en |
dc.subject | disease exacerbation | en |
dc.subject | fatality | en |
dc.subject | immunocompetent cell | en |
dc.subject | innate immunity | en |
dc.subject | interferon production | en |
dc.subject | lymphocytic choriomeningitis | en |
dc.subject | lymphocytopenia | en |
dc.subject | macrophage function | en |
dc.subject | mouse | en |
dc.subject | nonhuman | en |
dc.subject | priority journal | en |
dc.subject | protein deficiency | en |
dc.subject | protein expression | en |
dc.subject | protein function | en |
dc.subject | signal transduction | en |
dc.subject | spleen | en |
dc.subject | vesicular stomatitis | en |
dc.subject | virus immunity | en |
dc.subject | virus infection | en |
dc.subject | virus replication | en |
dc.subject | Animalia | en |
dc.subject | Lymphocytic choriomeningitis virus | en |
dc.subject | Mus | en |
dc.subject | Vesicular stomatitis virus | en |
dc.title | Deficiency of the B cell-activating factor receptor results in limited CD169+ macrophage function during viral infection | en |
dc.type | journalArticle | en |
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