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STAT1 Signaling in CD8 T Cells Is Required for Their Clonal Expansion and Memory Formation Following Viral Infection In Vivo¹

Michael Quigley, Xiaopei Huang^* and Yiping Yang^2,*,

^* Department of Medicine and Department of Immunology, Duke University Medical Center, Durham, NC 27710

Recent advances have shown that direct type I IFN signaling on T cells is required for their efficient expansion in response to viral infections in vivo. It is not clear which intracellular signaling molecule is responsible for this effect. Although STAT1 has been shown to mediate many of the type I IFN-dependent biological effects, its role in T cells remains uncertain in vivo. In this study, we demonstrated that STAT1 signaling in CD8 T cells was required for their efficient expansion by promoting the survival of activated CD8 T cells upon vaccinia viral infection in vivo, suggesting that the direct effect of type I IFNs on CD8 T cells is mediated by STAT1. Furthermore, effector CD8 T cells that lack STAT1 signaling did not survive the contraction phase to differentiate into long-lived memory cells. These results identify a critical role for type I IFN-STAT1 signaling in multiple stages of CD8 T cell response in vivo and suggest that strategies to activate type I IFN-STAT1 signaling pathway may enhance vaccine potency.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by Grants CA111807 and CA047741 from the National Institutes of Health, and an Alliance for Cancer Gene Therapy grant (to Y.Y.).

² Address correspondence and reprint requests to Dr. Yiping Yang, Department of Medicine, Duke University Medical Center, Box 103005, Durham, NC 27710. E-mail address: yang0029{at}mc.duke.edu

³ Abbreviations used in this paper: VV, vaccinia virus; HA, hemagglutinin; WT, wild type.

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