Spontaneous and glucocorticoid-induced apoptosis in human mature T lymphocytes.
Blood
; 86(11): 4199-205, 1995 Dec 01.
Article
en En
| MEDLINE
| ID: mdl-7492778
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.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Dexametasona
/
Linfocitos T
/
Apoptosis
Límite:
Humans
Idioma:
En
Revista:
Blood
Año:
1995
Tipo del documento:
Article
País de afiliación:
Italia
Pais de publicación:
Estados Unidos