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* Section of Biochemistry and Molecular Biology, Department of Orthopedic Surgery, and Departments of
Internal Medicine,
Immunology/Microbiology, and
Biochemistry, Rush University at Rush-Presbyterian-St. Luke’s Medical Center, Chicago, IL 60612;
¶ Department of Anatomy and Cell Biology, University of Western Ontario, London, Ontario, Canada; and
|| Institute of Biochemistry, University of Lausanne, Epalinges, Switzerland
Activation-induced cell death (AICD) of T cells is one of the major mechanisms of peripheral tolerance. The regulation of AICD by IL-4 is poorly understood. In this study, we report that AICD in IL-4-deficient T cells is significantly reduced compared with that in wild-type T cells. This impaired AICD correlates with the failure to induce degradation of cellular FLIP. IL-4-mediated enhancement of AICD and cellular FLIP degradation requires a Janus kinase/STAT-6 signaling pathway. Unexpectedly, these effects of IL-4 could be blocked by a neutralizing anti-IL-2 Ab, and addition of rIL-2 could completely restore the defective AICD in IL-4-deficient T cells. Furthermore, IL-4 regulates the T cell thresholds for IL-2 signaling during AICD. These data suggest that IL-4 promotes AICD via an IL-2-dependent mechanism.
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