Elucidation of the mechanism and significance of TGF-beta3 production in CD4+ T cells

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K19568
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Collagenous pathology/Allergology
• Research Institution: The University of Tokyo
• Principal Investigator: IWASAKI YUKIKO 東京大学, 医学部附属病院, 助教 (30592935)
• Research Collaborator: Teruya Shuzo 東京大学, 医学部附属病院アレルギーリウマチ内科, 大学院生
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: 制御性T細胞 / TGF-beta3 / IL-27 / IL-6 / p28 / Ebi3

Outline of Final Research Achievements

LAG3+ Treg, a peripherally-inducible Treg, is reported to show suppressive function through production of TGF-beta3. We have reported that IL-27 can induce TGF-beta3 on mouse naive CD4+ T cell, being endowed with suppressive function. IL-27 consists of p28 and Ebi3, each of which is suggested to have its own function. Interestingly, IL-27+IL-6+p28+Ebi3 combination was the strongest stimuli to induce TGF-beta3 mRNA expression. Moreover, TGF-beta3 mRNA expression was deeply suppressed in p28 or Ebi3 deficient LAG3+ Treg.

Free Research Field

膠原病