Role of Sox molecules in the development of autoimmune diseases

2016 Fiscal Year Final Research Report

• Project/Area Number: 26461461
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Collagenous pathology/Allergology
• Research Institution: Chiba University
• Principal Investigator: Suto Akira 千葉大学, 大学院医学研究院, 特任准教授 (50447306)
• Co-Investigator(Kenkyū-buntansha): 鈴木 浩太郎 千葉大学, 医学部附属病院, 講師 (90554634)
• Co-Investigator(Renkei-kenkyūsha): NAKAJIMA Hiroshi 千葉大学, 大学院医学研究院, 教授 (00322024)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: Sox12 / 自己免疫性腸炎

Outline of Final Research Achievements

We have previously shown that Sox5 and c-Maf cooperatively induce Th17 cell differentiation via the induction of RORγt as downstream targets of Stat3. However, the role of other Sox family molecules in the development of autoimmune diseases was still largely unknown. Here, we show that the expression of Sox12, a member of SoxC family, is significantly induced in Treg cells under inflammatory conditions. Although Sox12 is not required for the development of nTreg cells, Sox12 is involved in the development of pTreg cells under inflammatory conditions in adoptive transfer colitis models. Moreover, we found that enforced expression of Sox12 is sufficient to promote Foxp3 expression in CD4+ T cells even in the absence of TGF-β or IL-2 and that Sox12 binds to Foxp3 promoter and drives its transcription.

Free Research Field

アレルギー　膠原病