Identification of regulatory B cells in vivo and elucidation of its suppressive mechanism

2015 Fiscal Year Final Research Report

• Project/Area Number: 24689023
• Research Category: Grant-in-Aid for Young Scientists (A)
• Allocation Type: Partial Multi-year Fund
• Research Field: Immunology
• Research Institution: Osaka University
• Principal Investigator: Yoshihiro Baba 大阪大学, 免疫学フロンティア研究センター, 特任准教授 (20415269)
• Project Period (FY): 2012-04-01 – 2016-03-31
• Keywords: 制御性B細胞 / 炎症 / 自己免疫疾患 / IL-10

Outline of Final Research Achievements

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 factor Blimp1 in B lineage cells developed an exacerbated EAE. Hence, plasmablasts in the dLNs serve as IL-10 producers to limit autoimmune inflammation. As with mice, we established that human plasmablasts derived from naive B cells selectively secreted IL-10, reinforcing the importance of plasmablasts as IL-10-producing regulatory cells.

Free Research Field

免疫