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Interferon Is Required for Activation-induced Death of T Lymphocytes

¹ Department of Pathology, University of California San Francisco, San Francisco, CA 94143
² Center for Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139

Address correspondence to Abul K. Abbas, Department of Pathology, University of California San Francisco, 505 Parnassus Ave., M590, San Francisco, CA 94143-0506. Phone: 415-514-0681; Fax: 415-502-4563; E-mail: aabbas{at}itsa.ucsf.edu

The effector cytokine interferon (IFN-) may play a role in T cell homeostasis. We have examined the requirement for IFN- in one mechanism that regulates T cell expansion and survival, activation-induced cell death (AICD). CD4⁺ T cells lacking IFN- or the Stat1 transcription factor are resistant to AICD. IFN- is required for the production of caspases, and retrovirus-mediated expression of caspase-8 restores the sensitivity of Stat1-deficient T cells to AICD. In vitro, IFN- limits the expansion of T cells that are stimulated through their antigen receptors. Thus, IFN- may function to control the expansion and persistence of T cells by promoting caspase-8–dependent apoptosis.

Key Words: apoptosis • IFN- • Fas • caspases • Stat1

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