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- W1562642500 abstract "STAT3 regulates CD4<sup >+</sup> T cell survival and differentiation. However, its effects on CD8<sup >+</sup> T cells are not well understood. Here, we show that in comparison to WT CD8<sup >+</sup> T cells, STAT3-deficient CD8<sup >+</sup> 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), <svg style=vertical-align:-3.27599pt;width:48.474998px; id=M1 height=20.8375 version=1.1 viewBox=0 0 48.474998 20.8375 width=48.474998 xmlns:xlink=http://www.w3.org/1999/xlink xmlns=http://www.w3.org/2000/svg> <g transform=matrix(.017,-0,0,-.017,.062,16.7)><path id=x70 d=M169 380l92 53q26 16 49 16q80 0 128.5 -56t48.5 -133q0 -108 -72.5 -180.5t-176.5 -91.5q-38 1 -69 18v-131q0 -57 13 -70t71 -18v-27h-236v27q49 5 61 17t12 61v452q0 48 -9.5 58.5t-56.5 16.5v24q66 11 145 43v-79zM169 346v-270q37 -39 94 -39q63 0 101.5 50
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t-108.5 38.5q-44 0 -56 -12q-11 -8 -11 -47z /></g><g transform=matrix(.012,-0,0,-.012,44.052,7.8)><use xlink:href=#x31/></g> </svg>, Bcl-2, OX-40, and upregulation of FasL, Bax, and Bad. We examined whether STAT3-deficient CD8<sup >+</sup> 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-<svg style=vertical-align:-3.56265pt;width:8.6374998px; id=M3 height=12.175 version=1.1 viewBox=0 0 8.6374998 12.175 width=8.6374998 xmlns:xlink=http://www.w3.org/1999/xlink xmlns=http://www.w3.org/2000/svg> <g transform=matrix(.017,-0,0,-.017,.062,7.675)><path id=x1D6FE d=M478 372q0 -39 -31 -97t-61 -98t-78 -98q-45 -55 -73 -102q-13 -79 -13 -197q-11 -11 -43.5 -25.5t-53.5 -15.5l-15 17q5 35 26 101.5t47 123.5q8 72 -1.5 174.5t-37.5 178.5q-14 37 -29 37q-20 0 -67 -65l-25 21q37 60 73 90.5t63 30.5q47 0 72 -112q13 -56 17.5 -141.5
t0.5 -143.5h2q155 193 155 297q0 26 -12 47q-5 8 -5 15q0 16 12.5 27t29.5 11q21 0 34 -21t13 -55z /></g> </svg> and virus-specific KLRG-1<sup >+</sup> CD8<sup >+</sup> 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<sup >+</sup> 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<sup >+</sup> 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." @default.
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- W1562642500 title "STAT3 Regulates Proliferation and Survival of CD8<sup>+</sup>T Cells: Enhances Effector Responses to HSV-1 Infection, and Inhibits IL-10<sup>+</sup>Regulatory CD8<sup>+</sup>T Cells in Autoimmune Uveitis" @default.
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