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The Journal of Immunology, 1999, 163: 3131-3137.
Copyright © 1999 by The American Association of Immunologists

The Role of the Common Cytokine Receptor {gamma}-Chain in Regulating IL-2-Dependent, Activation-Induced CD8+ T Cell Death1

Zhenhua Dai, Alexandr Arakelov, Maylene Wagener, Bogumila T. Konieczny and Fadi G. Lakkis2

The Carlos and Marguerite Mason Transplantation Research Center, Renal Division, Department of Medicine, Veterans Affairs Medical Center and Emory University, Atlanta, GA 30033

IL-2-dependent, activation-induced T cell death (AICD) plays an important role in peripheral tolerance. Using CD8+ TCR-transgenic lymphocytes (2C), we investigated the mechanisms by which IL-2 prepares CD8+ T cells for AICD. We found that both Fas and TNFR death pathways mediate the AICD of 2C cells. Neutralizing IL-2, IL-2R{alpha}, or IL-2Rß inhibited AICD. In contrast, blocking the common cytokine receptor {gamma}-chain ({gamma}c) prevented Bcl-2 induction and augmented AICD. IL-2 up-regulated Fas ligand (FasL) and down-regulated {gamma}c expression on activated 2C cells in vitro and in vivo. Adult IL-2 gene-knockout mice displayed exaggerated {gamma}c expression on their CD8+, but not on their CD4+, T cells. IL-4, IL-7, and IL-15, which do not promote AICD, did not influence FasL or {gamma}c expression. These data provide evidence that IL-2 prepares CD8+ T lymphocytes for AICD by at least two mechanisms: 1) by up-regulating a pro-apoptotic molecule, FasL, and 2) by down-regulating a survival molecule, {gamma}c.




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