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目的 :证实SLE患者T细胞功能异常是否与其生物化学信号传导异常有关以及EGTA对其影响 ,探讨SLE的发病机理。方法 :用CD3单抗与羊抗鼠二抗IgG相交联刺激T细胞并用EGTA干预后 ,分别粘附细胞仪连续观察 10minT细胞 [Ca2 + ]i的变化 ,并评价 [Ca2 + ]i反应与CD3分子的相关性。结果 :正常人和SLE患者T细胞 [Ca2 + ]i反应的基准值相似 (P =0 .10 5 ) ;SLE患者高峰值、平台值T细胞的 [Ca2 + ]i反应明显高于正常对照 (P <0 .0 0 1,P <0 .0 0 1) ;加入EGTA后二者 [Ca2 + ]i反应有显著差异 :二者的T细胞CD3阳性率无差异 (P =0 .6 6 5 )。结论 :SLE患者T细胞TCR/CD3介导的信号转导途径存在异常 ,且不受EGTA的影响 ,可能是贮存库 [Ca2 + ]i释放的增加所致。
Objective: To confirm whether SLE patients with T cell dysfunction and its biochemical signaling abnormalities related to EGTA and its impact on the pathogenesis of SLE. Methods: T cells were stimulated with CD3 McAb and goat anti-mouse secondary IgG and treated with EGTA. The changes of [Ca2 +] i in T cells were observed by adherent cells and the expression of [Ca2 +] i and CD3 Correlation of molecules. Results: The baseline values of [Ca2 +] i responses of T cells in normal and SLE patients were similar (P = 0.105). The response of [Ca2 +] i in high and platform T cells of SLE patients was significantly higher than that of normal controls P <0.01, P <0.01). There was a significant difference in [Ca2 +] i response between EGTA and EGTA after adding EGTA: there was no difference in the positive rate of CD3 between the two groups (P = 0.665 ). CONCLUSION: TCR / CD3-mediated signal transduction pathway of T cells in SLE patients is abnormal and not affected by EGTA, which may be due to the increased release of [Ca2 +] i in the reservoir.