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Fas-mediated apoptosis of CD4+ and CD8+ T cells from human immunodeficiency
virus-infected persons: differential in vitro preventive effect of
cytokines and protease antagonists
J Estaquier, M Tanaka, T Suda, S Nagata, P Golstein and JC Ameisen
Inserm U415, Lille, France.
Human immunodeficiency syndrome (HIV) infection leads to a progressive loss
of T-cell-mediated immunity associated with T-cell apoptosis. We report
here that CD4+ and CD8+ T cells from HIV-1-infected persons are sensitive
to Fas (CD95/APO-1)-mediated death induced either by an agonistic anti-Fas
antibody or by the physiologic soluble Fas ligand, although showing no
sensitivity to tumor necrosis factor alpha-induced death. CD4+ and CD8+
T-cell apoptosis induced by Fas ligation was enhanced by inhibitors of
protein synthesis and was prevented either by a soluble Fas receptor decoy
or an antagonistic anti-Fas antibody. Fas- mediated apoptosis could also be
prevented in a CD4+ or CD8+ T-cell- type manner (1) by several protease
antagonists, suggesting the involvement of the interleukin-1beta
(IL-1beta)-converting enzyme (ICE)- related cysteine protease in CD4+
T-cell death and of both a CPP32- related cysteine protease and a calpain
protease in CD8+ T-cell death; and (2) by three cytokines, IL-2, IL-12, and
IL-10, that exerted their effects through a mechanism that required de novo
protein synthesis. Finally, T-cell receptor (TCR)-induced apoptosis of CD4+
T cells from HIV-infected persons involved a Fas-mediated death process,
whereas TCR stimulation of CD8+ T cells led to a different Fas-independent
death process. These findings suggest that Fas-mediated T-cell death is
involved in acquired immunodeficiency syndrome (AIDS) pathogenesis and that
modulation of Fas-mediated signaling may represent a target for new
therapeutic strategies aimed at the prevention of CD4+ T-cell death in
AIDS.
Volume 87,
Issue 12,
pp. 4959-4966,
06/15/1996
Copyright © 1996 by The American Society of Hematology
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