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Spontaneous and glucocorticoid-induced apoptosis in human mature T
lymphocytes
M Brunetti, N Martelli, A Colasante, M Piantelli, P Musiani and FB Aiello
Department of Human Pathology, G. D'Annunzio University, Chieti, Italy.
Glucocorticoid (GC)-induced apoptosis is a well-recognized physiologic
regulator of murine T-cell number and function. We have analyzed its
mechanisms in human mature T cells, which have been thought to be
insensitive until recently. Peripheral blood T cells showed sensitivity to
GC-induced apoptosis soon after the proliferative response to a mitogenic
stimulation, and were also sensitive to spontaneous (ie, growth factor
deprivation-dependent) apoptosis. CD8+ T cells were more sensitive to both
forms than CD4+ T cells. Acquisition of sensitivity to GC-induced apoptosis
was not associated with any change in number or affinity of GC receptors.
Both spontaneous and GC-induced apoptosis were increased by the
macromolecular synthesis inhibitors, cycloheximide (CHX) and puromycin. A
positive correlation between the degree of protein synthesis inhibition and
the extent of apoptosis was observed. Interleukin-2 (IL-2) IL-4, and IL-10
protected (IL-2 > IL-10 > IL-4) T cells from both forms of apoptosis
in a dose-dependent manner. Our data suggest that spontaneous and
GC-induced apoptosis regulate the human mature T-cell repertoire by acting
early after the immune response and differentially affecting T-cell
subsets.
Volume 86,
Issue 11,
pp. 4199-4205,
12/01/1995
Copyright © 1995 by The American Society of Hematology
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