Interleukin-2 programs mouse alpha beta T lymphocytes for apoptosis.
Antigen receptor stimulation of mature alpha beta T lymphocytes can lead either to proliferation or death. Programmed cell death, termed apoptosis, leads to the clonal deletion of both thymocytes and mature T cells that establishes tolerance. 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 V beta 8+ 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.
Lenardo
M J
MJ
Laboratory of Immunology, National Institute for Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892.
D000818:Animals; D015704:CD4 Antigens / Q000502:physiology*; D016923:Cell Death / Q000187:drug effects*; D002455:Cell Division; D002999:Clone Cells; D005434:Flow Cytometry; D007376:Interleukin-2 / Q000494:pharmacology*; D051379:Mice; D015375:Receptors, Interleukin-2 / Q000187:drug effects / Q000502:physiology; D016176:T-Lymphocyte Subsets / Q000166:cytology / Q000276:immunology; D013601:T-Lymphocytes / Q000166:cytology* / Q000187:drug effects / Q000276:immunology
D015704:CD4 Antigens; D007376:Interleukin-2; D015375:Receptors, Interleukin-2