【摘要】 目的原发性系膜增生性肾炎(MsPGN)的发病机制和糖皮质激素(GC)耐药机制虽然部分已明确,但其确切机制仍未阐明。细胞毒性T淋巴细胞相关抗原(CTLA-4)是T细胞活化的重要抑制性分子。本研究探讨MsPGN患儿外周血淋巴细胞CTLA-4表达和淋巴细胞凋亡及地塞米松(Dex)对其影响。方法分别采用直接免疫荧光、流式细胞仪及AnnexinV-FITC/PI双染流式细胞仪检测Dex处理或非Dex处理的MsPGN组和对照组体外培养外周血淋巴细胞膜CTLA-4的表达和其凋亡。结果体外培养MsPGN组淋巴细胞CTLA-4的自然表达和Dex诱导的表达均较对照组低(P<0.05);MsPGN组淋巴细胞自然凋亡和Dex诱导的凋亡亦较对照组低(P<0.05),且两者均呈正相关性(P<0.05)。结论CTLA-4表达异常可能参与了MsPGN的发病机制及GC耐药机制。更多还原

【Abstract】 Objective The pathogenesis of mesangial proliferative glomerulonephritis(MsPGN)and mechanisms of glucocorticoid(GC)resistance have not been fully identified.Cytotoxic T-lymphocyte antigen-4(CTLA-4)is an important inhibitor of T-lymphocyte activation.The objective of the study is to investigate the CTLA-4 expression and apoptosis in lymphocytes of children with MsPGN and the effects of dexamethasone(Dex)on the CTLA-4 expression and apoptosis.Methods Blood samples were collected from 36 children with MsPGN and 30 healthy children.CTLA-4 expression in in vitro cultured lymphocytes with or without Dex treatment was measured by flow cytometry following direct immune fluorescene.The rate of apoptosis in the lymphocytes was evaluated by annexin V-FITC and propidium iodide staining.Results The CTLA-4 expression and apoptosis in lymphocytes from children with MsPGN were significantly lower than those in the healthy control children in the absence or presence of Dex treatment(P<0.05).There was a positive correlation between CTLA-4 expression and apoptosis in lymphocytes(P<0.05).Conclusions Abnormal CTLA-4 expression may participate in the pathogenesis of MsPGN and be one of mechanisms of GC resistance.更多还原