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CD2 rescues T cells from T-cell receptor/CD3 apoptosis: a role for the
Fas/Fas-L system
E Ayroldi, G Migliorati, L Cannarile, R Moraca, DV Delfino and C Riccardi
Department of Clinical Medicine, Pathology, and Pharmacology, Perugia
University, Medical School, Italy.
Anti-CD3 monoclonal antibodies (MoAbs) and glucocorticoid hormones induce
apoptosis in immature thymocytes and peripheral T lymphocytes. This process
is inhibited by a number of growth factors, including interleukin-2 (IL-2),
IL-3, and IL-4, as well as by triggering of the adhesion molecule CD44,
which would indicate that signals generated by membrane receptors can
modulate the survival of lymphoid cells. To investigate whether triggering
of CD2 may also affect apoptosis in lymphoid cells, we analyzed the effect
of stimulation with anti-CD2 MoAbs on T-cell apoptosis induced by two
stimuli, anti-CD3 MoAbs and dexamethasone (DEX), using a hybridoma T-cell
line and a T-helper cell clone. The results show that CD2 engagement
decreased anti-CD3 MoAb- induced apoptosis, but did not influence
DEX-induced cell death. Furthermore, the decrease appeared to be related to
the expression of Fas/APO-1 (CD95) and Fas-ligand (Fas-L). In fact, we show
that CD2 stimulation inhibits apoptosis by preventing the CD3-induced
upregulation of Fas and Fas-L in a Fas-dependent experimental system. These
data suggest that a costimulatory molecule may control a deletion pathway
and may therefore contribute to the regulation of peripheral tolerance.
Volume 89,
Issue 10,
pp. 3717-3726,
05/15/1997
Copyright © 1997 by The American Society of Hematology
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