Distinct roles of IL-1 and IL-6 in human T cell activation.

Distinct roles of IL-1 and IL-6 in human T cell activation.
复制标题

IL-1 和 IL-6 在人类 T 细胞激活中的不同作用。

DOI:
--
复制
发表时间:
1989
影响因子:
4.4
通讯作者:
J. V. Snick
J. V. Snick
中科院分区:
医学2区
文献类型:
--
作者:
F. Houssiau;Pierre Coulie;J. V. Snick

文献摘要

被引文献

相似文献

我们已经研究了IL-1和IL-6激活人T细胞的机制。我们报告说,PHA刺激的辅助细胞耗尽扁桃体T细胞的基础上,其密度分级显示高度的异质性,在他们的增殖反应,这些细胞因子,因为小致密淋巴细胞基本上没有响应,而大细胞广泛增殖。这种不同的反应可以归因于这样的事实,即在这些情况下,只有大细胞产生IL-2,从而提供了明确的证据,在IL-1和IL-6激活人T细胞的IL-2介导的步骤的存在。发现IL-1和IL-6之间的协同作用是由于它们对IL-2的产生和对IL-2的应答的互补作用,其中IL-1在诱导IL-2中起主要作用,并且除了IL-1之外,IL-6是最佳IL-2应答所需的。使用小扁桃体T细胞,有可能表明,伴随着对IL-2的增强反应,IL-6诱导细胞大小和蛋白质合成的显着增加。在没有其他因素的情况下,这种活化之后没有进入S期,这表明IL-6在T细胞活化中的重要作用是诱导细胞从G 0移动到G1,在那里它们变得对IL-1诱导的少量IL-2更敏感。
We have examined the mechanisms underlying the activation of human T cells by IL-1 and IL-6. We report that PHA-stimulated accessory cell-depleted tonsillar T cells fractionated on the basis of their density show a high degree of heterogeneity in their proliferative response to these cytokines, inasmuch as small dense lymphocytes essentially fail to respond whereas large cells proliferate extensively. This differential response could be ascribed to the fact that only the large cells produced IL-2 under these circumstances, thus providing unequivocal evidence for the existence of an IL-2-mediated step in the activation of human T cells by IL-1 and IL-6. The synergy between IL-1 and IL-6 was found to result from their complementary effects on the production of and response to IL-2, with IL-1 playing a preponderant role in the induction of IL-2, and IL-6 being required, in addition to IL-1, for optimal IL-2-responsiveness. Using small tonsillar T cells, it was possible to show that, concomitant with the enhanced response to IL-2, IL-6 induced a marked increase in cell size and in protein synthesis. In the absence of other factors, this activation was not followed by entry into S phase, suggesting that the essential role of IL-6 in T cell activation is to induce the cells to move from G0 to G1, where they become more responsive to the small amounts of IL-2 induced by IL-1.