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糖皮质激素对SLE患者CD4^+,CD8^+T细胞Caspase-3及TRAIL受体基因表达的影响 被引量:1

Effects of glucocorticoid therapy on the expression of Caspase-3 and TRAIL receptors in CD4^+ and CD8^+ T cells of patients with systemic lupus erythematosus
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摘要 目的探讨糖皮质激素对系统性红斑狼疮(SLE)患者CD4^+.CD8^+T淋巴细胞Caspase-3及肿瘤坏死因子相关凋亡诱导配体(TRAIL)受体基因表达的影响。方法免疫磁珠法分离20例糖皮质激素治疗前后SLE患者及10例正常人对照的外周血CD4^+,CD8^+T淋巴细胞,半定量逆转录聚合酶链反应(RT-PCR)分析其Caspase-3及TRAIL受体mRNA的表达。结果SLE患者治疗后CD4^+T淋巴细胞TRAIL-R1表达显著降低(P〈0.05);SLE患者治疗前后CD8^+T细胞Caspase-3的表达显著高于正常人对照(P值分别〈0.01和〈0.05);SLE患者治疗前CD8^+T细胞TRAIL-R2的表达显著高于正常人对照(P〈0.05)。结论通过调节SLE患者T细胞TRAIL受体表达以抑制其凋亡可能是糖皮质激素治疗SLE的机制之一。 Objective To investigate the effects of glucocorticoid therapy on the gene expression of Caspase-3 and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptors in CD4^+ and CD8^+ T cells of patients with systemic lupus erythematosus ( SLE ). Methods Peripheral blood CD4^+ and CD8^+ T cells of 20 SLE patients before and after prednisone therapy and 10 healthy volunteers were isolated with a magnetic cell sorting system ( MACS ). The expression of Caspase-3 and TRAIL receptors mRNA in the CD4^+ and CD8^+ T cells were detected by semiquantitative reverse transcriptase-polymerase chain reaction ( RT-PCR ). Results The TRAIL-R1 expression in CD4^+ T cells of SLE patients significantly declined after therapy ( P 〈 0.05 ). The Caspase-3 expression of CD8^+ T cells in SLE patients before and after therapy was significantly higher than that in healthy controls ( P〈 0.01, P〈 0.05, respectively). The CD8^+ T cells from SLE patients before therapy showed significantly increased expression of TRAIL-R2 compared with those from healthy volunteers ( P 〈 0.05 ). Conclusion These findings suggest that inhibiting T cell apoptosis through regulation of the expression of TRAIL receptors may be one of the mechanisms of glucocortieoid for treatment of SLE.
出处 《中华皮肤科杂志》 CAS CSCD 北大核心 2007年第1期19-21,共3页 Chinese Journal of Dermatology
基金 国家自然科学基金资助项目(30271199).
关键词 红斑狼疮 系统性 天胱氨酸天冬氨酸蛋白酶 糖皮质激素类 肿瘤坏死因子相关凋亡诱导配件 Lupus erythematosus, systemic Caspases Glucocorticoids Tumor necrosis factor-related apoptosis -inducing ligand
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