The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1997/12/1939/ $5.00
The Journal of Experimental Medicine, Volume 186, Number 11, December 1, 1997 1939-1944

Brief Definitive Reports

T Cell Receptor Signals Enhance Susceptibility to Fas-mediated Apoptosis

Brian Wong, Joseph Arron, and Yongwon Choi*

From the * Howard Hughes Medical Institute, The Rockefeller University, New York 10021

Fas(CD95) and its ligand (FasL) interaction plays a pivotal role in T cell receptor (TCR)-mediated apoptosis. However, the susceptibility of T cells to Fas-mediated apoptosis is tightly regulated during immune responses, a regulation which is thought to maintain the antigen-specificity of T cell apoptosis. Here we show that TCR stimulation enhances the induction of Fas-mediated apoptosis. In addition, using a mutant T cell hybridoma with impaired FasL expression, we show that the synergy provided by TCR stimulation can be mimicked by activators of PKC but not calcium influx. This effect cannot be inhibited by actinomycin D, suggesting that TCR stimulation leads to the alteration in preexisting signaling molecules to enhance Fas-mediated apoptosis. Our results therefore provide a mechanism of how Fas-FasL interactions lead to T cell death in an antigen-specific manner via repetitive antigen stimulation.

Address correspondence to Yongwon Choi, Ph.D., HHMI, The Rockefeller University, 1230 York Ave., Box 295, New York, NY 10021. Phone: 212-327-7441; Fax: 212-327-7319; E-mail: choi{at}rockvax.rockefeller.edu

Note added in proof. After this paper was accepted for publication, we found that Hornung et al. also reported that TCR signals can increase Fas-mediated apoptosis (Hornung, S., L. Zheng, and M.J. Lenardo. 1997. J. Immunol. 159:3816–3822).


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