作者: M Brunetti , N Martelli , A Colasante , M Piantelli , P Musiani
DOI: 10.1182/BLOOD.V86.11.4199.BLOODJOURNAL86114199
关键词:
摘要: 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 been thought to be insensitive until recently. Peripheral blood cells showed sensitivity GC-induced soon after the proliferative response mitogenic stimulation, were also sensitive spontaneous (ie, growth factor deprivation-dependent) apoptosis. CD8+ more both forms than CD4+ cells. Acquisition was not associated with any change or affinity GC receptors. Both increased by macromolecular synthesis inhibitors, cycloheximide (CHX) puromycin. A positive correlation between degree protein inhibition extent observed. Interleukin-2 (IL-2) IL-4, IL-10 protected (IL-2 > IL-4) from dose-dependent manner. Our data suggest that regulate repertoire acting early immune differentially affecting subsets.