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机构地区:[1]深圳市人民医院(暨南大学第二临床医学院)临床医学研究中心,深圳518020 [2]深圳市人民医院风湿免疫科,深圳518020
出 处:《中国免疫学杂志》2006年第11期1048-1051,共4页Chinese Journal of Immunology
基 金:广东省自然科学基金(No.021339)资助
摘 要:目的探讨γδT细胞在系统性红斑狼疮疾病中的免疫保护作用。方法检测17例正常人群和44例系统性红斑狼疮患者外周血γδT细胞及亚群的表达情况。以TCRγδ单克隆抗体固相法体外选择性扩增获得17例活动期系统性红斑狼疮患者和10例正常人群外周血TCRγδ细胞系。测定γδT细胞毒活性。用正常人群γδT细胞系与异体活动期SLE患者外周血单核细胞(PMBC)以1∶5、1∶10比例共同培养48小时,活动期SLE患者PMBC作对照孔,观察γδT细胞系对活动期SLE患者PMBC活化和凋亡、细胞因子分泌的影响。结果SLE患者的γδT细胞及亚群数量明显减少(P<0.05)。IL-2可显著增强γδT细胞的细胞毒作用。正常人γδT细胞系与异体SLE活动期患者PMBC细胞共同培养,共同培养二组SLE患者PMBC的CD69表达和凋亡率均较对照组明显下降(P<0.01)。共同培养二组培养上清IL-10水平较对照组明显升高,具有明显差异(P<0.05)。结论SLE患者γδT细胞数及亚群较正常人群明显下降,γδT细胞对SLE外周血淋巴细胞的凋亡和活化具有抑制性作用,并使IL-10分泌水平升高,表明γδT细胞在SLE发病中具有保护性的免疫调节作用。Objective:To study the protective effect of γδT cells in systemic lupus erythematosus. Methods:TotalγδT cells, Vδ1 , Vδ2, Vδ3 and VT9 subsets in peripheral blood from 17 normal control ,44 active systemic lupus erythematosus (SLE) patients were examined by using cytometry assay. High purified γδT cell lines were established by stimulation of immobilized anti-TCRγδ monoclonal antibody in vitro. γδT cell cytotoxic activity was observed. The peripheral blood mononuclear cells from active SLE patients were cocultured with γδT cell lines from normal control for 48 h by 1 : 5 and 1 : 10 ratio. PBMC from same active SLE patient was the control group. The influence of TCRγδ cell lines on apoptosis and activity of peripheral blood mononuclear from patients with systemic lupus erythematosus was observed. Results :The number of γδT cells and subsets in SLE patients were remarkably decreased comparison with the normal controls( P 〈 0. 05 ). Their cytotoxicites were significantly enhanced by IL-2. The apoptosis and expression CD69 of peripheral blood mononuclear from patients with systemic lupus erythematosus from co-cultured groups were significantly lower than those of control group( P 〈 0. 05 ). Secretion of IL-10 by co-cultured groups was significantly higher than that of control group, it was significant differences( P 〈 0. 05 ). Conclusion:γδT cells may be inhibiting apoptosis and activity on PBMC from SLE.
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