中华皮肤科杂志 ›› 2007, Vol. 40 ›› Issue (1): 19-21.

• 论著 • 上一篇    下一篇

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

游弋1, 郝飞1, 邓永键2   

  1. 1. 第三军医大学西南医院皮肤科 重庆 400038;
    2. 南方医科大学南方医院病理科
  • 收稿日期:2006-02-20 出版日期:2007-01-15 发布日期:2007-01-15
  • 通讯作者: 郝飞,email:haofei@mail.tmmu.com.cn E-mail:haofei@mail.tmmu.com.cn
  • 基金资助:
    国家自然科学基金资助项目(30271199)

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

YOU Yi1, HAO Fei1, DENG Yong-jian2   

  1. Department of Dennatology, Southwest Hospital, the Third Military Medical University, Chongqing 400038, China
  • Received:2006-02-20 Online:2007-01-15 Published:2007-01-15

PDF (PC)

51

赞

摘要： 目的 探讨糖皮质激素对系统性红斑狼疮(SLE)患者CD4+,CDB+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.

关键词: 沙眼衣原体, 抗菌药, 药敏实验, 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体

Abstract: 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-Rl 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 glucocorticoid for treatment of SLR.

Key words: Lupus erythematosus, systemic, Caspases, Glucocorticoids, Tumor necrosis factor-related apoptosis-inducing ligand