2012 Fiscal Year Final Research Report

SOCS1 Is One of the Key Molecules to Prevent the Plasticity of Regulatory T Cells and the Development of Autoimmunity

Research Project

Project/Area Number	23791121
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
Research Field	膠原病・アレルギー・感染症内科学
Research Institution	防衛医科大学校 (2012) National Defense Medical College (2011)
Principal Investigator	TAKAHASHI Reiko 防衛医科大学校, 医学教育部医学科専門課程, 助教 (90422120)
Project Period (FY)	2011 – 2012
Keywords	全身性エリテマトーデス / 制御性T細胞
Research Abstract	Recently, natural Foxp3+ T cells have been shown to be a heterogeneous population regarding developmental plasticity. We have shown that T cell specific SOCS1 deficient (LckCre-SOCS1-flox) mice show autoimmune phenotypes, and Tregs from LckCre-SOCS1-flox mice easily convert into Th1- or Th17-like cells, which lack Foxp3 expression and suppressive functions in vivo. Because Tregs in LckCre-SOCS1-flox mice were constantly exposed to inflammatory cytokines from non-Treg cells in vivo, we then analyzed Treg specific SOCS1 deficient mice (Foxp3Cre-SOCS1-flox). When Tregs from Foxp3Cre-SOCS1-flox mice were cultured with antigen presenting cells from LckCre-SOCS1-flox mice, they produced IFN ・amma, which indicate SOCS1 deficient Tregs develop plasticity under conditions in which APCs were highly activated.

(5 results)