【摘要】 目的　明确激素敏感型肾病综合征T淋巴细胞致病因子的亚群来源 ,探讨CD+ 4T淋巴细胞在本病发病中的作用。方法　采用间接免疫荧光染色法测定肾病综合征患儿外周血CD+ 4、CD+ 8T细胞百分率 ,以及CD+ 4/CD+ 8比值 ;磺柳酸比浊法测定经大鼠尾静脉注射抗体结合 补体介导溶解法分离的患儿CD+ 4和CD+ 8T淋巴细胞培养上清液后的大鼠尿蛋白含量 ,电镜观察其肾小球超微结构与基底膜上阴离子位点改变。结果　 (1)肾病综合征活动期患儿外周血CD+ 4T淋巴细胞百分率为(33 4± 2 4) % ,与正常儿童比较差异无显著性 (P >0 0 5 ) ;CD+ 8T淋巴细胞百分率为 (15 5±4 5 ) % ,比正常儿显著降低 (P <0 0 1) ;CD+ 4/CD+ 8比值为 (2 2± 0 3) % ,比正常儿显著升高(P <0 0 1)。(2 )注射患儿CD+ 4T淋巴细胞培养上清液后 ,大鼠尿蛋白排泌量在 0～ 8h时间段由注射前的 (3 9± 0 6 )mg/ 2 4h显著增加到 (13 1± 4 3)mg/ 2 4h(P <0 0 0 1)。注射患儿CD+ 8T淋巴细胞培养上清液后 ,大鼠尿蛋白排泌量无明显变化 (P >0 0 5 )。蛋白尿大鼠出现肾小球上皮细胞足突融合、基底膜上阴离子位点显著减少。结论　注射患儿CD+ 4T淋巴细胞培养上清液可使大鼠出现一过性蛋白尿 ;CD+ 4T淋巴细胞功能紊乱 ,分泌致病因子是激素敏感型肾病综合更多还原

【Abstract】 Objective It has been well proved that the products of T lymphocytes play the most important role in steroid sensitive nephrotic syndrome (SSNS), but the subset of T cells relateal to the disease remains to be identified. In this study, the authors separated and cultured the CD + 4 and CD + 8 T cells from SSNS patients, and examined their effects on the protein secretion in wistar rats to characterize the pathogenic role of T cell subset in SSNS. Methods Indirect immune fluorescence method was used to examine the percentages of the CD + 4 and CD + 8 T cell in the peripheral blood from children with SSNS. Separated CD + 4 and CD + 8 T cell were cultured, and supernants were injected into the wistar rats′ tail veins. Then the changes in the amount of the animals′ uric protein were observed Results (1) In the acute phase of SSNS, the percentage of CD + 8 T cell decreased significantly (from 29.2± 5.0 to 15.5±4.5, P < 0.01), while that of the CD + 4 T cell did not change ( P >0.05),the ratio of CD + 4/CD + 8 increased from 1.3 ± 0.8 to 2.2±0.3, P < 0.01. (2)The injection of the cultured superstants from CD + 4 T cells resulted in remarkable increase of the uric protein′s amount within 8 hours after injection [from (3.9±0.6) mg/24 h to (13.1±4.3) mg/24 h, P <0.001], while those from CD + 8 T cells did not influence the uric protein′s quantity ( P >0.05). In addition, there were obvious changes in the glomerular ultrastructure of the rats that received CD + 4 T cell superstants and had proteinuria, including the decreasing of the anions on their glomerular basement membrane and the fuse of the epithelial cell foot, which did not occur in those injected with CD + 4 T cell products. Conclusion Injection of the supernatants of the cultured CD + 4 T cells from children with SSNS induced transient proteinuria in rats, whose glomerular ultrastructure had the same alteration as SSNS patients. These findings provided obvious evidence that the major pathogenic factor may come from CD + 4 T lymphocyte.更多还原