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Interleukin-10-producing plasmablasts exert regulatory function in autoimmune inflammation


Matsumoto, M; Baba, A; Yokota, T; Nishikawa, H; Ohkawa, Y; Kayama, H; Kallies, A; Nutt, SL; Sakaguchi, S; Takeda, K; Kurosaki, T; Baba, Y
2014-12-18
Immunity
Journal Article
41
6
1040-51
B cells can suppress autoimmunity by secreting interleukin-10 (IL-10). Although subpopulations of splenic B lineage cells are reported to express IL-10 in vitro, the identity of IL-10-producing B cells with regulatory function in vivo remains unknown. By using IL-10 reporter mice, we found that plasmablasts in the draining lymph nodes (dLNs), but not splenic B lineage cells, predominantly expressed IL-10 during experimental autoimmune encephalomyelitis (EAE). These plasmablasts were generated only during EAE inflammation. Mice lacking plasmablasts by genetic ablation of the transcription factors Blimp1 or IRF4 in B lineage cells developed an exacerbated EAE. Furthermore, IRF4 positively regulated IL-10 production that can inhibit dendritic cell functions to generate pathogenic T cells. Our data demonstrate that plasmablasts in the dLNs serve as IL-10 producers to limit autoimmune inflammation and emphasize the importance of plasmablasts as IL-10-producing regulatory B cells.
Cell Press
Molecular Immunology
10.1016/j.immuni.2014.10.016
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Creation Date 2015-03-12 03:59:01 Last Modified 2015-03-16 09:13:28