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

Masanori Matsumoto, Akemi Baba, Takafumi Yokota, Hiroyoshi Nishikawa, Yasuyuki Ohkawa, Hisako Kayama, Axel Kallies, Stephen L. Nutt, Shimon Sakaguchi, Kiyoshi Takeda, Tomohiro Kurosaki, Yoshihiro Baba

Research output: Contribution to journalArticlepeer-review

240 Citations (Scopus)

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 invitro, the identity of IL-10-producing B cells with regulatory function invivo 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 Tcells. 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.

Original languageEnglish
Pages (from-to)1040-1051
Number of pages12
JournalImmunity
Volume41
Issue number6
DOIs
Publication statusPublished - Dec 18 2014

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

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