International Immunology, Vol 10, 175-183, Copyright © 1998 by Oxford University Press
Y Yang, D Kim and CG Fathman
Activation of T cell hybridomas in vitro induces rapid Fas-Fas ligand
(FasL)-mediated programmed cell death (apoptosis). In contrast, T cells
activated by antigen or superantigen in vivo undergo a population expansion
and then decline due to Fas-FasL-mediated activation-induced apoptosis
(AIA). We asked how T cells activated by antigen in vivo proliferated
before undergoing apoptosis. Two possibilities were analyzed: either (i)
the apoptosis program was not 'turned on' or (ii) was 'blocked' during the
period of cellular proliferation in vivo. Data presented in this manuscript
support the second of these possibilities. CD4+ T cells activated in vivo
were resistant to anti-fas-mediated apoptosis until 48 h following
staphylococcal enterotoxin B (SEB) administration, despite the fact that
activated proliferating T cells expressed high levels of Fas (CD95) antigen
and many 'apoptosis genes' were induced within 24 h of SEB administration.
The analysis of the expression patterns of 'apoptosis genes' during the T
cell activation further suggested that temporal blockade of AIA may be due
to the induction of apoptosis-preventing genes, such as bag-1.
ARTICLES
Regulation of programmed cell death following T cell activation in vivo
Department of Medicine, Stanford University School of Medicine, CA 94305-5111, USA.
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