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Suppressor of TCR signaling-2 (STS-2) suppresses arthritis development in mice.

Mod Rheumatol. 2018 Jul;28(4):626-636. doi:10.1080/14397595.2017.1380249. Epub 2017 Oct 03
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摘要


OBJECTIVES:Suppressor of TCR signaling-2 (STS-2) is one of the RA susceptibility genes identified in genome-wide association studies (GWAS). We tried to verify the involvement of STS-2 on the development of autoimmune arthritis in a mouse model. METHODS:STS-2 knock-out (KO) and wild type (WT) mice were immunized with chicken type II collagen (CII). For CD4+ helper T cell (Th) subset analysis, intracellular cytokines in splenocytes and lymph node cells were stained and analyzed by flow cytometry. Regulatory T cell (Treg) function was analyzed by co-culturing effector CD4+T cells and Tregs collected from non-immunized mice. RESULTS:CII-immunized STS-2 KO mice developed arthritis more frequently than WT mice. Although the T cell activation profile and Th subset in spleen and LNs were similar between STS-2 KO and WT mice, STS-2 KO mice showed increased IL-2-producing CD4+T cells in spleen when compared with WT mice. Accordingly, STS-2 KO CD4+T cells promoted IL-2 production by TCR stimulation. However, STS-2 KO Tregs normally suppressed T cell proliferation. CONCLUSION:We proved that STS-2 is involved in the arthritis development by collagen-induced arthritis. Higher IL-2 production from STS-2 KO T cells is suggested to have a main pathogenic role in arthritis development.

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