Regulation of inflammatory cytokine signaling by TRAF5

2017 Fiscal Year Final Research Report

• Project/Area Number: 15H04640
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Biological pharmacy
• Research Institution: University of Toyama (2017); Tohoku University (2015-2016)
• Principal Investigator: SO TAKANORI 富山大学, 大学院医学薬学研究部(薬学), 教授 (60294964)
• Co-Investigator(Kenkyū-buntansha): 奥山 祐子 東北大学, 医学系研究科, 助教 (50624475) ; 石井 直人 東北大学, 医学系研究科, 教授 (60291267)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 炎症 / サイトカイン / TNF

Outline of Final Research Achievements

IL-17-producing helper CD4+ T cells, Th17 cells, control not only host defense against pathogens but also immune pathogenesis of inflammatory and autoimmune diseases. Th17 cells differentiate from antigen-primed naive CD4+ T cells in response to IL-6, and the IL-6-receptor signaling plays a dominant role for the development of Th17 cells. In this study, we found that TRAF2 and TRAF5 associated with the signal-transducing receptor gp130 expressed by naive CD4+ T cells differentially regulated the instructive IL-6-receptor signaling that is needed for the development of Th17 cells.

Free Research Field

免疫学