The role of caspase 3 and BclxL in the action of interleukin 7 (IL-7):: A survival factor in activated human T cells
The role of caspase 3 and BclxL in the action of interleukin 7 (IL-7):: A survival factor in activated human T cells
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DOI：
10.1006/cyto.1998.0351
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发表时间：
1998-09-01
期刊：
影响因子：
3.8
通讯作者：
Dobson, PRM
中科院分区：
文献类型：
--
作者：
Amos, CL;Woetmann, A;Dobson, PRM
研究了白细胞介素7（IL-7）对白细胞介素2（IL-2）依赖的活化的原代人T淋巴细胞（hT细胞）凋亡的影响。两种细胞因子均能抑制地塞米松诱导的Caspase 3的激活，并阻止Caspase 3的底物聚ADP核糖聚合酶（PARP）的裂解。IL-7能上调Bcl x（L）的表达，并对抗地塞米松对Bcl x（L）的下调。Bcl-2蛋白表达上调IL-7与或没有地塞米松，但Bcl-2的表达水平比BclxL在这些细胞中低得多。Bas水平在细胞因子刺激或地塞米松治疗后均无显著变化。一个未鉴定的23-kDa条带被抗Bcl-2抗体识别，被地塞米松诱导，并被IL-7和IL-2抑制。与p26 Bcl-2蛋白相比，该蛋白受到独立的调节，这表明它可能是一个新的因子，可能参与细胞凋亡的调节，IL-7作为细胞因子撤出和糖皮质激素诱导的活化的原代hT细胞凋亡的存活因子的明确作用是有牵连的。此外，Bclx（L）的调节和Caspase 3活性的下游抑制可能介导这种拯救信号。(C)北京：科学出版社.
The effects of interleukin 7 (IL-7) on apoptosis in interleukin 2 (IL-2)-dependent, activated, primary, human T lymphocytes (hT cells) was examined, IL-7 (like IL-2) rescued cells from apoptosis, as measured by their cellular DNA profile and fragmentation. IL-2 also acted as a mitogen in these T cells, Both cytokines abrogated the dexamethasone-induced stimulation of Caspase 3 and prevented the cleavage of poly (ADP-ribose) polymerase (PARP), a substrate for Caspase 3, IL-7 upregulated the expression of Bclx(L) and counteracted the downregulation of this anti-apoptotic protein by the synthetic glucocorticoid, dexamethasone. Bcl-2 protein expression was upregulated by IL-7 with or without dexamethasone, but Bcl-2 was expressed at a much lower level than BclxL in these cells. Levels of Bas did not markedly change on either cytokine stimulation or dexamethasone treatment. An unidentified 23-kDa band, which was recognized by the anti-Bcl-2 antibody, was induced by dexamethasone and suppressed by IL-7 and IL-2, This protein was subject to independent regulation as compared to the p26 Bcl-2 protein, suggesting that it may be a novel factor, possibly involved in the regulation of apoptosis, A clear role for IL-7 as a survival factor for cytokine withdrawal and glucorcorticoid induced apoptosis in activated primary hT cells is implicated. In addition, regulation of Bclx(L) and downstream inhibition of Caspase 3 activity may mediate this rescue signal. (C) 1998 Academic Press.