IDDM患者T细胞受体介导的信号通路受损

Defect of TCR-mediated signal pathway of Tcells in IDDM patients

目的 :进一步研究IDDM患者T细胞应答改变的机制。方法 :用抗TCR抗体激活患者外周血T细胞 ,分析TCR介导的信号通路的水平。结果 :与正常对照组相比较 ,抗TCR抗体诱导的增殖性应答较弱 (P <0 .0 5) ;rIL 2能部分恢复对抗TCR抗体应答的缺乏 ;抗CD2 8抗体刺激不能恢复TCR介导的增殖性应答 (P =0 .0 3 )。结论 :IDDM患者的T细胞对抗TCR抗体应答的缺乏与TCR介导的信号通路受损有关 ,但协同刺激信号通路正常。

AIM: To study the mechanism responsible for alteration of T cell respons e in IDDM patients. METHODS: T cells from peripheral blood of I DDM patients were activated by anti-TCR antibodies. The level of TCR-mediated signaling pathway was analyzed. RESULTS: T cells from IDDM patients responded weakly to anti- TCR antibody-induced proliferation, as compared with T cells from normal subjec ts (P< 0.05) . The defect could be partially remedied by the addition of rIL-2, while the anti-CD28 antibody stimulation did not restore the prolifera tive response of anti-TCR-induced cells from IDDM patients(P=0.03). CONCLUSION: Underresponsiveness of the T cells from IDDM patients to anti-TCR antibody may result from a defect in the signaling pathway, the CD28 c o-stimulation-signaling pathway is normal. Defect in the TCR signaling pathwa y increases the sensitivity of T cells from IDDM patients to apoptosis or anergy .