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目的 探讨超抗原诱导T细胞无能的分子机制。方法 采用ELISA和FACS ,分别检测超抗原对诱导T细胞无能的过程中 ,IL 2、IL 10的产生和IL 2Rα链 (CD2 5 )的表达 ,并以3 H TdR掺入法 ,测定无能T细胞对rhIL 2、PMA及iono mycin的应答能力。 结果 在诱导T细胞无能的过程中 ,IL 2的产生显著降低 ,而IL 10的产生则逐渐升高 ;CD2 5的表达与活化组相比较无显著差异。rhIL 2的加入可恢复T细胞增殖 ;PMA单独作用能诱导无能T细胞的部分增殖能力 ,但PMA +ionomycin则能更大程度地恢复T细胞的增殖。结论 超抗原SEA对T细胞无能的诱导 ,可能与降低IL 2的水平和升高IL 10的水平有关。超抗原SEA的反复刺激对T细胞无能的诱导 ,可能是干扰了TCR信号途径的近端事件 ,导致Ras/MAPK途径和Ca/calcineurin途径受阻 ,而使IL 2基因不能转录所致
Objective To investigate the molecular mechanism of superantigen-induced T cell incompetence. Methods The production of IL 2 and IL 10 and the expression of IL-2Rα chain (CD25) during the induction of inability of T cells by superantigen were detected by ELISA and FACS respectively. T cell incompetence Response to rhIL 2, PMA and ionomycin. Results In the process of inducing T cell impotence, the production of IL 2 was significantly decreased, while the production of IL 10 was gradually increased. The expression of CD25 was not significantly different from that of the activated group. The addition of rhIL 2 restored the proliferation of T cells; PMA alone induced partial proliferation of implanted T cells, but PMA + ionomycin restored the proliferation of T cells to a greater extent. Conclusion The induction of T cell incompetence by superantigen SEA may be related to the decrease of IL 2 level and the increase of IL 10 level. Repeated stimulation of the superantigen SEA on T cells induced impotence may interfere with the proximal events of the TCR signaling pathway, resulting in the obstruction of the Ras / MAPK pathway and the Ca / calcineurin pathway, leaving the IL 2 gene unable to be transcribed