tetano
Editor, Senior Moderator
J Immunol. 2017 Jul 26. pii: ji1700560. doi: 10.4049/jimmunol.1700560. [Epub ahead of print]
[h=1]sIgM-FcμR Interactions Regulate Early B Cell Activation and Plasma Cell Development after Influenza Virus Infection.[/h] Nguyen TTT[SUP]1,[/SUP][SUP]2[/SUP], Graf BA[SUP]3[/SUP], Randall TD[SUP]3[/SUP], Baumgarth N[SUP]4,[/SUP][SUP]2,[/SUP][SUP]5[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Previous studies with mice lacking secreted IgM (sIgM) due to a deletion of the μs splice region (μs[SUP]-/-[/SUP] ) 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[SUP]-/-[/SUP] mice. B cell-specific Fcmr[SUP]-/-[/SUP] 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[SUP]-/-[/SUP] but not Fcmr[SUP]-/-[/SUP] 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
[h=1]sIgM-FcμR Interactions Regulate Early B Cell Activation and Plasma Cell Development after Influenza Virus Infection.[/h] Nguyen TTT[SUP]1,[/SUP][SUP]2[/SUP], Graf BA[SUP]3[/SUP], Randall TD[SUP]3[/SUP], Baumgarth N[SUP]4,[/SUP][SUP]2,[/SUP][SUP]5[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Previous studies with mice lacking secreted IgM (sIgM) due to a deletion of the μs splice region (μs[SUP]-/-[/SUP] ) 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[SUP]-/-[/SUP] mice. B cell-specific Fcmr[SUP]-/-[/SUP] 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[SUP]-/-[/SUP] but not Fcmr[SUP]-/-[/SUP] 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