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Cutting Edge: Contributions of Apoptosis and Anergy to Systemic T Cell Tolerance¹

Department of Pathology, University of California, San Francisco, CA 94143

Multiple pathways can induce and maintain peripheral T cell tolerance. The goal of this study was to define the contributions of apoptosis and anergy to the maintenance of self-tolerance to a systemic Ag. Upon transfer into mice expressing OVA systemically, OVA-specific DO11 CD4⁺ T cells are activated transiently, cease responding, and die. Bim is the essential apoptosis-inducing trigger and apoptosis proceeds despite increased expression of Bcl-2 and Bcl-x. However, preventing apoptosis by eliminating Bim does not restore proliferation or cytokine production by DO11 cells. While Foxp3 is transiently induced, anergy is not associated with the stable development of regulatory T cells. Thus, apoptosis is dispensable for tolerance to a systemic self-Ag and cell-intrinsic anergy is sufficient to tolerize T cells.

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 Grant PO1 AI35297.

² Address correspondence and reprint requests to Dr. Abul K. Abbas, Department of Pathology, University of California, San Francisco, CA 94143. E-mail address: Abul.Abbas{at}ucsf.edu

³ Abbreviations used in this paper: Treg, regulatory T cell; sOVA Tg, soluble OVA transgenic; HPRT, hypoxanthine phosphoribosyltransferase; WT, wild type.

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