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sIgM-FcμR Interactions Regulate Early B Cell Activation and Plasma Cell Development after Influenza Virus Infection

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  • sIgM-FcμR Interactions Regulate Early B Cell Activation and Plasma Cell Development after Influenza Virus Infection

    J Immunol. 2017 Jul 26. pii: ji1700560. doi: 10.4049/jimmunol.1700560. [Epub ahead of print]
    sIgM-FcμR Interactions Regulate Early B Cell Activation and Plasma Cell Development after Influenza Virus Infection.

    Nguyen TTT1,2, Graf BA3, Randall TD3, Baumgarth N4,2,5.
    Author information

    Abstract

    Previous studies with mice lacking secreted IgM (sIgM) due to a deletion of the μs splice region (μs-/- ) had shown sIgM involvement in normal B cell development and in support of maximal Ag-specific IgG responses. Because of the changes to B cell development, it remains unclear to which extent and how sIgM directly affects B cell responses. In this study, we aimed to explore the underlying mechanisms of sIgM-mediated IgG response regulation during influenza virus infection. Generating mice with normally developed μs-deficient B cells, we demonstrate that sIgM supports IgG responses by enhancing early Ag-specific B cell expansion, not by altering B cell development. Lack of FcμR expression on B cells, but not lack of Fcα/μR expression or complement activation, reduced antiviral IgG responses to the same extent as observed in μs-/- mice. B cell-specific Fcmr-/- mice lacked robust clonal expansion of influenza hemagglutinin-specific B cells early after infection and developed fewer spleen and bone marrow IgG plasma cells and memory B cells, compared with controls. However, germinal center responses appeared unaffected. Provision of sIgM rescued plasma cell development from μs-/- but not Fcmr-/- B cells, as demonstrated with mixed bone marrow chimeric mice. Taken together, the data suggest that sIgM interacts with FcμR on B cells to support early B cell activation and the development of long-lived humoral immunity.
    Copyright ? 2017 by The American Association of Immunologists, Inc.


    PMID: 28747342 DOI: 10.4049/jimmunol.1700560
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