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Guy’s, King’s and St. Thomas’ School of Medicine, Rayne Institute, London, United Kingdom
Correspondence: Alistair Noble, Department of Immunology, Rayne Institute, 123 Coldharbour Lane, London, SE5 9NU, U.K. E-mail: alistair.noble{at}kcl.ac.uk
Human primary effector T cells were analyzed for their susceptibility
to anti-CD3-induced activation-induced cell death (AICD). Th1 and Tc1
cells were more susceptible to AICD than their type 2 counterparts.
Type 1 and type 2 subsets were also found to be differentially
susceptible to CD95-mediated apoptosis, although cell-surface
expression of CD95 and CD95L was at similar levels on all subsets. A
role for CD95 in AICD was confirmed by the addition of anti-CD95L
antibodies that partially abrogated AICD. Residual apoptosis could not
be accounted for by TNF-
/TNFR interactions because although type 1
cells secreted more TNF- than type 2 cells, the addition of TNFR:Fc
fusion protein did not inhibit AICD. Instead, a reduction in AICD was
observed in the presence of EGTA or concanamycin A. The inhibition of
apoptosis by a granzyme B inhibitor z-AAD-CMK in Tc1 cells further
indicated an involvement of the granule exocytosis mechanism in
AICD.
Key Words: apoptosis • CD4+ • CD8+ • TNFR • perforin
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