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

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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.