The elucidation of mechanism of differentiation of regulatory B cells and autoantibody-producing cells from B-1 cells

2021 Fiscal Year Final Research Report

• Project/Area Number: 20K16288
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 49070:Immunology-related
• Research Institution: Kyushu University
• Principal Investigator: Hatano Shinya 九州大学, 生体防御医学研究所, 助教 (90834929)
• Project Period (FY): 2020-04-01 – 2022-03-31
• Keywords: B細胞 / 加齢性B細胞 / 自己抗体 / 自己免疫疾患

Outline of Final Research Achievements

Because I couldn't establish the originally planned B cell fate tracking system for fetuses, I used the the already established adult mouse B cell fate tracking system and I worked on the study of Age-Associated B Cells that were reported to increase in aged mice and are involved in autoantibody production. As a result, I identified gene X, which is highly expressed in long-lived B cells of aged mice as compared to B cells of young mice. In addition, the protein expression of gene X was not observed in B cells of young mice and was detected in B cells of aged mice. These results suggested that gene X is a novel marker that defines a subset of Age-Associated B Cells.

Free Research Field

免疫学

Academic Significance and Societal Importance of the Research Achievements

B細胞は生体防御の中でも抗体産生など液性免疫の要となる細胞であるが、老化により液性免疫応答が低下することが報告されており、その原因は不明な点が多い。近年、加齢に伴い増加する特殊なB細胞サブセットであり、自己抗体産生に関与する加齢性B細胞が報告されたが、加齢性B細胞を規定するマーカーは詳細に同定されていない。本研究成果により、加齢性B細胞の新規マーカーとなりうる遺伝子Xの同定に成功した。この研究成果は今後の加齢性B細胞の機能や性状、自己免疫疾患への関与、そして老化による液性免疫応答低下メカニズムの詳細な解明に繋がる可能性があり、超高齢化社会における健康寿命の延長に寄与することが期待される。