Tuosto L, Cundari E, Gilardini Montani M S, Piccolella E
Department of Cellular and Developmental Biology, University La Sapienza, Rome, Italy.
Eur J Immunol. 1994 May;24(5):1061-5. doi: 10.1002/eji.1830240508.
We present evidence that dexamethasone (Dex), a synthetic glucocorticosteroid, causes apoptosis in mature human T cells, similarly to what has been reported for murine T lymphocytes. Human T cell clones and short-term activated T lymphocytes treated with Dex show the characteristic pattern of apoptotic cells, such as hypodiploid nuclei, chromatin condensation and DNA fragmentation into oligonucleosomal fragments. However, Dex susceptibility of T cells to apoptosis is cell cycle-dependent. The progression in the proliferative cell cycle (G1 versus S) rescues Dex-treated T cells from apoptosis. Moreover, occupancy of the T cell receptor reverses Dex-induced apoptotic phenomena. These observations suggest that glucocorticoids contribute to the regulation of the proliferative or the suicidal response of antigen-activated human T cells.
我们提供的证据表明，合成糖皮质激素地塞米松（Dex）可导致成熟人类T细胞凋亡，这与之前报道的鼠T淋巴细胞情况类似。用Dex处理的人类T细胞克隆和短期活化的T淋巴细胞呈现出凋亡细胞的特征模式，如亚二倍体细胞核、染色质浓缩以及DNA断裂成寡核小体片段。然而，T细胞对Dex诱导凋亡的敏感性是细胞周期依赖性的。增殖细胞周期（G1期与S期）的进展可使经Dex处理的T细胞免于凋亡。此外，T细胞受体的占据可逆转Dex诱导的凋亡现象。这些观察结果表明，糖皮质激素有助于调节抗原激活的人类T细胞的增殖或自杀反应。
