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1996-02-27
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Document 0574
DOCN M9630574
TI Spontaneous and glucocorticoid-induced apoptosis in human mature T
lymphocytes.
DT 9603
AU Brunetti M; Martelli N; Colasante A; Piantelli M; Musiani P; Aiello FB;
Department of Human Pathology, G. D'Annunzio University, Chieti,; Italy.
SO Blood. 1995 Dec 1;86(11):4199-205. Unique Identifier : AIDSLINE
MED/96082175
AB 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.
DE Apoptosis/*DRUG EFFECTS Cell Differentiation
Cycloheximide/PHARMACOLOGY CD4-Positive T-Lymphocytes/CYTOLOGY/DRUG
EFFECTS CD8-Positive T-Lymphocytes/CYTOLOGY/DRUG EFFECTS
Dexamethasone/*PHARMACOLOGY Human In Vitro Lymphocyte Transformation
Protein Synthesis Inhibitors/PHARMACOLOGY Puromycin/PHARMACOLOGY
Support, Non-U.S. Gov't T-Lymphocytes/*CYTOLOGY/*DRUG
EFFECTS/IMMUNOLOGY JOURNAL ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).