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实验性非洲锥虫病中T细胞激活抑制因子及白细胞介素2活性降低

Suppressor factor of T-cell activation and decreased interleukin 2 activity in experimental African trypanosomiasis.

作者信息

Alcina A, Fresno M

出版信息

Infect Immun. 1985 Nov;50(2):382-7. doi: 10.1128/iai.50.2.382-387.1985.

Abstract

Spleen cells from Trypanosoma brucei-infected BALB/c mice were unable to respond to a T-cell mitogen, concanavalin A. Moreover, they were unable to produce detectable amounts of the growth factor required for T cell proliferation, interleukin 2. In addition, supernatants from 24-h in vitro cultures of these cells produced a slight but detectable suppressive activity of the interleukin 2-dependent proliferation of a T-cell line. Infected spleen cells also suppressed the response of T. brucei-immunized spleen cells as well as normal spleen cells to concanavalin A. However, a major difference was shown in the mechanism of the suppression in both systems. Suppression of normal spleen cells required cell-to-cell contact. In contrast, suppression of 30-day T. brucei-immune cells could be mediated by a soluble suppressor factor released by in vitro culture of infected spleen cells. This molecule had an apparent molecular weight of 18,000. Finally, similar suppression could be generated in 30-day T. brucei-immune spleen cells but not in normal cells, with living cells but not with extracts of T. brucei.

摘要

来自感染布氏锥虫的BALB/c小鼠的脾细胞无法对T细胞丝裂原刀豆球蛋白A作出反应。此外,它们无法产生可检测量的T细胞增殖所需的生长因子白细胞介素2。另外,这些细胞体外培养24小时后的上清液对T细胞系的白细胞介素2依赖性增殖产生了轻微但可检测到的抑制活性。受感染的脾细胞还抑制了布氏锥虫免疫的脾细胞以及正常脾细胞对刀豆球蛋白A的反应。然而,在这两个系统中抑制机制显示出主要差异。对正常脾细胞的抑制需要细胞间接触。相比之下,对30天布氏锥虫免疫细胞的抑制可由感染脾细胞体外培养释放的可溶性抑制因子介导。该分子的表观分子量为18,000。最后,活的布氏锥虫而非其提取物可在30天布氏锥虫免疫的脾细胞中产生类似的抑制作用,但在正常细胞中则不会。

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