Rapamycin blocks IL-2-driven T cell cycle progression while preserving T cell survival
Rapamycin blocks IL-2-driven T cell cycle progression while preserving T cell survival
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DOI：
10.1006/bcmd.2001.0420
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发表时间：
2001-05-01
影响因子：
2.3
通讯作者：
Prystowsky, MB
中科院分区：
文献类型：
--
作者：
Gonzalez, J;Harris, T;Prystowsky, MB
有效的细胞免疫应答需要抗原特异性T淋巴细胞的增加; IL-2驱动抗原刺激的T细胞增殖，并且主要负责观察到的增加。我们使用含有近似9000个小鼠cDNA的微阵列来研究IL-2诱导的基因表达。IL-2诱导调节细胞周期进程、控制细胞存活以及增加增殖期间的合成和代谢过程的基因的表达。IL-2还抑制阻断细胞周期进程和促进细胞死亡的基因的表达。雷帕霉素通过下调细胞周期进程所需的关键过程所需的基因表达来抑制IL-2驱动的增殖。雷帕霉素还通过保持IL-2诱导的细胞存活程序的完整性来保持细胞存活。这些基因表达的复杂多面程序允许细胞增殖和细胞存活的动态调节。(C)北京：科学出版社.
Effective cellular immune responses require increases in antigen-specific T lymphocytes; IL-2 drives antigen-stimulated T cell proliferation and is largely responsible for the increases observed. We used microarrays containing similar to 9000 mouse cDNAs to study IL-2-induced gene expression. IL-2 induces the expression of genes that regulate cell cycle progression, control cell survival, and increase synthetic and metabolic processes during proliferation. IL-2 also suppresses expression of genes that block cell cycle progression and promote cell death. Rapamycin inhibits IL-2-driven proliferation by downregulating the expression of genes required for key processes required for cell cycle progression. Rapamycin also preserves cell survival by keeping intact the IL-2-induced cell survival programs. These complex multifaceted programs of gene expression permit a dynamic regulation of cellular proliferation and cellular survival. (C) 2001 Academic Press.