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J. Exp. Med.,
Volume 187, Number 8, April 20, 1998 1179-1192
Association
By
From the * Department of Immunology, Fundación Jiménez-Díaz, Avenida Reyes Católicos 2, 28040 Madrid, Spain; We have previously shown that a tyrosine to leucine replacement in the transmembrane region
of T cell receptor (TCR)- Departamento de Bioquímica y Biologia Molecular I, Universidad Complutense
de Madrid, Spain; and § Centro de Biología Molecular Severo Ochoa, CSIC-Universidad Autónoma
de Madrid, Cantoblanco, 28049 Madrid, Spain
results in a deficient induction of CD95-L and apoptosis upon
TCR triggering in a transfected T cell line. By contrast, interleukin (IL)-2 production and the
expression of CD25 and CD69 were normally induced. Since the mutation in TCR- also resulted in impaired association of CD3-
, it was proposed that this chain is specifically required for the induction of apoptosis. We now show that the deficient induction of CD95-L and apoptosis does not derive from a general lower production of second messengers, since intracellular
Ca2+ fluxes and tyrosine phosphorylation of total proteins were elicited at wild-type levels.
Unlike in T cell clones stimulated with partial agonists, both p21 and p18 forms of tyrosine-phosphorylated CD3- were detected, although the overall level of tyrosine-phosphorylated CD3- was low. More strikingly, inducible association of ZAP70 to CD3- was strongly inhibited, despite a normal induction of ZAP70 tyrosine phosphorylation. Finally, ZAP70 was
not concentrated near the plasma membrane in the apoptosis-deficient cells. These results suggest that CD3- is necessary for engagement of a specific signaling pathway leading to CD95-L
expression that also needs the recruitment of ZAP70.
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