白介素2抑制T细胞特异性免疫应答机制的研究

Mechanism Underlying IL-2 Inhibition on T cell Specific Immune Response

本研究查明白介素2(IL-2)对静息T细胞抗原特异性免疫应答的作用,探讨IL-2对静息T细胞中细胞因子信号传导抑制蛋白(suppressor of cytokine signaling3,SOCS-3)表达的影响,及其与抗原特异性免疫应答的关系。用IL-2(50U/ml)预处理静息DO11.10T细胞,洗涤去除IL-2后用3H-TdR掺入法检测静息DO11.10T细胞针对OVA323-329抗原(ovalbumin,OVA,卵清蛋白)的特异性增殖;用IL-2(50U/ml)刺激静息DO11.10T细胞,然后用荧光实时定量PCR法检测SOCS-3在刺激后不同时间的表达变化;用OVA323-329抗原活化静息DO11.10T细胞,然后检测SOCS-3在抗原活化后不同时间的表达变化。结果表明:静息DO11.10T细胞经IL-2刺激后抗原特异性增殖能力减弱;静息DO11.10T细胞经IL-2刺激后SOCS-3表达上调,在刺激4小时后表达即明显上调,6小时后达到最高峰;静息DO11.10T细胞经OVA323-329抗原活化后SOCS-3表达明显下调,在活化后第2天降至最低,4天后基本恢复正常。结论:IL-2在一定条件下可抑制静息T细胞抗原特异性免疫应答,而且这种抑制作用可能与SOCS-3表达上调有关。

The study was aimed to investigate the effect of IL-2 on the acquired immune response of naive T cells, and to explore the influence of IL-2 on suppressor of cytokine signaling 3 （ SOCS-3 ） expression of naive T cells, as well as to elucidate the role of SOCS-3 on antigen specific immune response in vitro. Naive DO11. 10 T cells were prestimulated with IL-2 （50 U/ml）, and stimulated with OVA323 -329 antigen after removing IL-2, then the proliferation of naive DOll. 10 T cells was detected. Naive DOll. 10 T cells were stimulated with IL-2 （50 U/ml）, and SOCS-3 expression was detected by real-time PCR. Naive DO11, 10 T cells were stimulated with OVA323 -329 antigen, and SOCS- 3 expression was detected by means of 3H-TdR. The results showed that after IL-2 pre-stimulation, the proliferation of naive DOll. 10 T cells decreased significantly when stimulated with OVA323-329 antigen; SOCS-3 expression of naive DO11.10 T cells was up-regulated significantly after IL-2 stimulation, the up-regulation began obviously at 4 hours and reached peak at 6 hours. SOCS-3 expression on naive DO11.10 T cells was down-regulated markedly after OVA323 -329 antigen stimulation, the expression level of SOCS-3 was lowest on day 2 and returned to normal on day 4 after stimulation. It is concluded that the antigen specific immune response of naive DO11.10 T cells is inhabited after pre- stimulation with IL-2, which may be mediated by SOCS-3.