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目的 证实SLE患者T细胞功能异常是否与TCR/CD3 复合物介导的 [Ca2 + ]反应异常有关 ,以及 [Ca2 + ]i反应异常的原因。方法 用CD3 单抗与羊抗鼠二抗IgG相交联刺激T细胞并用Thapsigargin和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InsP3 生成量的相关性。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T细胞的 [Ca2 + ]i反应高峰值、平台值明显高于正常对照 (P <0 0 0 1,P <0 0 0 1) ;加入Thapsigargin后二者[Ca2 + ]i反应无显著差异 ,而加入EGTA后二者 [Ca2 + ]i反应有显著差异 ;二者的T细胞InsP3 生成量无差异 (P =0 5 3 7)。结论 SLE患者T细胞TCR/CD3 介导的 [Ca2 + ]i反应存在异常 ,这种 [Ca2 + ]i反应异常是储存库内Ca2 + 释放增加所致
Objective To confirm whether T cell dysfunction in patients with SLE is associated with an abnormal response of [Ca2 +] mediated by TCR / CD3 complex and the cause of abnormal response of [Ca2 +] i. Methods The T cells were stimulated by anti-mouse goat anti-mouse IgG with CD3 monoclonal antibody and intervened by Thapsigargin and EGTA respectively. The changes of [Ca2 +] i in T cells were observed by adherent cells and the [Ca2 +] i responses and Correlation of InsP3 production. Results The baseline values of [Ca2 +] i responses of T cells in normal and SLE patients were similar (P = 0 105). The peak value of [Ca2 +] i response in T cells of SLE patients was significantly higher than that of normal controls (P < There was no significant difference between the two [Ca2 +] i responses after addition of Thapsigargin, but there was a significant difference between [Ca2 +] i responses after addition of EGTA. Both T cells InsP3 There was no difference in the amount of production (P = 0 5 3 7). Conclusions TCR / CD3-mediated [Ca2 +] i responses in T cells of SLE patients are abnormal. This abnormality of [Ca2 +] i response is caused by the increase of Ca2 + release in the reservoir