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STAT3 regulates CD4 +  T cell survival and differentiation. However, its effects on CD8 +  T cells are not well understood. Here, we show that in comparison to WT CD8 +  T cells, STAT3-deficient CD8 +  T cells exhibit a preactivated memory-like phenotype, produce more IL-2, proliferate faster, and are more sensitive to activation-induced cell death (AICD). The enhanced proliferation and sensitivity to AICD correlated with downregulation of class-O forkhead transcription factors (FoxO1, FoxO3A), p21 waf1 , p27 KIP1 , Bcl-2, OX-40, and upregulation of FasL, Bax, and Bad. We examined whether STAT3-deficient CD8 +  T cells can mount effective response during herpes simplex virus (HSV-1) infection and experimental autoimmune uveitis (EAU). Compared to WT mice, HSV-1-infected STAT3-deficient mice (STAT3KO) produced less IFN- γ  and virus-specific KLRG-1 +  CD8 +  T cells. STAT3KO mice are also resistant to EAU and produced less IL-17-producing Tc17 cells. Resistance of STAT3KO to EAU correlated with marked expansion of IL-10-producing regulatory CD8 +  T cells (CD8-Treg) implicated in recovery from autoimmune encephalomyelitis. Thus, increases of IL-6-induced STAT3 activation observed during inflammation may inhibit expansion of CD8-Tregs, thereby impeding recovery from uveitis. These results suggest that STAT3 is a potential therapeutic target for upregulating CD8 +  T cell-mediated responses to viruses and suggest the successful therapeutic targeting of STAT3 as treatment for uveitis, derived, in part, from promoting CD8-Treg expansion.

mediators of inflammation

STAT3 Regulates Proliferation and Survival of CD8+T Cells: Enhances Effector Responses to HSV-1 Infection, and Inhibits IL-10+Regulatory CD8+T Cells in Autoimmune Uveitis