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Direct Interferon- Signaling Dramatically Enhances CD4⁺ and CD8⁺ T Cell Memory¹

The Scripps Research Institute, La Jolla, CA 92037

Studies in IFN--deficient mice suggest that the delivery of IFN- to CD8⁺ T cells early in virus infection programs their eventual contraction, thereby reducing the abundance of CD8⁺ memory T cells. In this study, we show that such mice fail to completely eliminate virus infection and that, when evaluated without the confounding factor of persisting Ag, both CD4⁺ and CD8⁺ T cells undergo profound contraction when they are unable to receive IFN- signals. Furthermore, the abundance of CD4⁺ and CD8⁺ memory cells that express the IFN- receptor is 100-fold higher than cells lacking this molecule. Thus, direct IFN- signaling is not required for T cell contraction during virus infection, and it enhances, rather than suppresses, the development of virus-specific CD4⁺ and CD8⁺ T cell memory.

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 National Institutes of Health Grants AI-27028 and AI-52351.

² Address correspondence and reprint requests to Molecular and Integrative Neurosciences Department, SP30-2110, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037. E-mail address: lwhitton{at}scripps.edu

³ Abbreviations used in this paper: LCMV, lymphocytic choriomeningitis virus; TSRI, The Scripps Research Institute; Tg, transgenic; WT, wild type; GKO mice, mice lacking IFN-; p.i., postinfection.

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