Deficiency of the B cell-activating factor receptor results in limited CD169+ macrophage function during viral infection
AuthorXu, H. C.; Huang, J.; Khairnar, V.; Duhan, V.; Pandyra, A. A.; Grusdat, M.; Shinde, P.; McIlwain, D. R.; Maney, S. K.; Gommerman, J.; Löhning, M.; Ohashi, P. S.; Mak, T. W.; Pieper, K.; Sic, H.; Speletas, M.; Eibel, H.; Ware, C. F.; Tumanov, A. V.; Kruglov, A. A.; Nedospasov, S. A.; Häusinger, D.; Recher, M.; Lang, K. S.; Lang, P. A.
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.
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