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lnterleukin-2 programs mouse αβ T lymphocytes for apoptosis

Nature volume 353, pages 858–861 (1991)Cite this article

Abstract

ANTIGEN receptor stimulation of mature αβ T lymphocytes can lead either to proliferation or death1–4. Programmed cell death, termed apoptosis, leads to the clonal deletion of both thymocytes and mature T cells that establishes tolerance5–9. How a mature T cell selects between proliferation and death is not understood. Here I show that interleukin-2 (IL-2) is a critical determinant of the choice between these two fates. Both CD4+ and CD8+ T cells previously exposed to IL-2 undergo apoptosis after antigen-receptor stimulation. Antibody blockade of IL-2 but not IL-4 reverses the marked reduction of lymph node Vβ8+ T cells caused in mice by the bacterial superantigen Staphylococcus aureus enterotoxin B. IL-2 may thus participate in a feedback regulatory mechanism by predisposing mature T lymphocytes to apoptosis.

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Authors and Affiliations

  1. Laboratory of Immunology, National Institute for Allergy and Infectious Diseases, National Institutes of Health, Bldg 10, Rm 11N311, Bethesda, Maryland, 20892, USA

    Michael J. Lenardo

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  1. Michael J. Lenardo
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Lenardo, M. lnterleukin-2 programs mouse αβ T lymphocytes for apoptosis. Nature 353, 858–861 (1991). https://doi.org/10.1038/353858a0

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