摘要
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
Aim To explore the molecular mechanism of T cell anergy induced by superantigen SEA. Methods The production of IL 2 and IL 10 and the expression of CD25 during the induction of T cell anergy were detected by ELISA and FACS respectively. Proliferation of anergic T cell response to rhIL 2, PMA and ionomycin stimulation were determined by 3H TdR incorporation. Results IL 2 production was reduced significantly, but IL 10 production was increased gradually during the induction of T cell anergy. Anergic T cells expressed normal level of CD25. Exogenous rhIL 2 could reversed anergic state of T cells. PMA alone could partially restored T cell proliferation, but the combination of PMA plus ionomycin could restore T cell proliferation more significantly than PMA alone. Conclusion The decrease of IL 2 level and the increase of IL 10 level probably contribute to the induction of T cell anergy. The repeated SEA stimulation results in a blocking of Ras/MAPK pathway and Ca/calcineurin pathway of TCR induced activation signal transduction, thus, make IL 2 gene fail to transcribe.
出处
《细胞与分子免疫学杂志》
CAS
CSCD
北大核心
2002年第6期536-538,共3页
Chinese Journal of Cellular and Molecular Immunology
基金
全军"九五"医药卫生科研重点基金资助No .96Z0 3 9
