| First Author | Nguyen TTT | Year | 2017 |
| Journal | J Immunol | Volume | 199 |
| Issue | 5 | Pages | 1635-1646 |
| PubMed ID | 28747342 | Mgi Jnum | J:254212 |
| Mgi Id | MGI:6100720 | Doi | 10.4049/jimmunol.1700560 |
| Citation | Nguyen TTT, et al. (2017) sIgM-FcmuR Interactions Regulate Early B Cell Activation and Plasma Cell Development after Influenza Virus Infection. J Immunol 199(5):1635-1646 |
| abstractText | Previous studies with mice lacking secreted IgM (sIgM) due to a deletion of the mus splice region (mus(-/-) ) 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 mus-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 FcmuR expression on B cells, but not lack of Fcalpha/muR expression or complement activation, reduced antiviral IgG responses to the same extent as observed in mus(-/-) 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 mus(-/-) but not Fcmr(-/-) B cells, as demonstrated with mixed bone marrow chimeric mice. Taken together, the data suggest that sIgM interacts with FcmuR on B cells to support early B cell activation and the development of long-lived humoral immunity. |
