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CD44 (Pgp-1) inhibits CD3 and dexamethasone-induced apoptosis
E Ayroldi, L Cannarile, G Migliorati, A Bartoli, I Nicoletti and C Riccardi
Department of Clinical Medicine, Pathology and Pharmacology, Perugia
University Medical School, Italy.
Anti-CD3 monoclonal antibodies (MoAbs) and glucocorticoid hormones (GCH)
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, indicating that signals generated by membrane
receptors can modulate the survival of lymphoid cells. To investigate
whether signals activated by adhesion receptors have a similar activity, we
analyzed the effect of CD44 (Pgp-1) adhesion molecule receptor stimulation
on T-cell apoptosis induced by three stimuli (anti-CD3 MoAbs, dexamethasone
[DEX] treatment, and exposure to ultraviolet irradiation [UV]) on a 3DO
T-cell line. The results show that CD44 engagement, either by hyaluronic
acid (HA) or anti-CD44 MoAbs, inhibits DNA fragmentation and apoptosis
induced by DEX and anti-CD3 MoAbs, whereas that induced by UV, a
p53-dependent phenomenon, was not inhibited. Furthermore, the antiapoptotic
effect exerted through CD44 activation does not seem related to
overexpression of bcl-2 or to have appreciable effects on cell
proliferation. Our results indicate that adhesion molecules modulate T-cell
survival by counteracting apoptosis induced by DEX or anti-CD3 MoAbs.
Volume 86,
Issue 7,
pp. 2672-2678,
10/01/1995
Copyright © 1995 by The American Society of Hematology
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