Interleukin-10-producing plasmablasts exert regulatory function in autoimmune inflammation
- Author(s)
- Matsumoto, M; Baba, A; Yokota, T; Nishikawa, H; Ohkawa, Y; Kayama, H; Kallies, A; Nutt, SL; Sakaguchi, S; Takeda, K; Kurosaki, T; Baba, Y;
- Details
- Publication Year 2014-12-18,Volume 41,Issue #6,Page 1040-51
- Journal Title
- Immunity
- Publication Type
- Journal Article
- Abstract
- 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.
- Publisher
- Cell Press
- Research Division(s)
- Molecular Immunology
- Publisher's Version
- https://doi.org/10.1016/j.immuni.2014.10.016
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2015-03-12 03:59:01
Last Modified: 2015-03-16 09:13:28