摘要
目的了解2剂赛尼哌治疗方案能够在1个月内完全阻断白细胞介素2受体(IL-2R),减少T细胞增殖,停用赛尼哌后是否还存在延续作用,除了IL-2R被阻断这个途径外是否还存在其他途径来调节免疫。方法对15例常规免疫抑制三联疗法(对照组)以及15例使用2剂赛尼哌诱导治疗(诱导组)的同种异体肾移植患者均随访6个月,每个患者均在术前2h,术后1个月,术后3个月以及术后6个月检查IL-2,IL-10,STAT5以及CD40L水平。结果术前2h、术后1个月、3个月以及6个月的IL-2,STAT5水平,诱导组和对照组间差异无统计学意义。IL-10水平在术后3个月时诱导组(59.4±7.7)ng/L明显高于对照组(36.8±8.4)ng/L。CD40L水平在术后1个月时诱导组(10.6±3.6)明显低于对照组(35.6±8.4)。结论赛尼哌能够在术后1个月时通过抑制CD40L水平来减少B细胞介导的体液免疫反应的发生。
Objective To determine whether there was any lingering effect after discontinuing Zenapax in renal transplantation and investigate there was any alternative immunity-regulating pathway of Zenapax other than IL-2/IL-2R. Methods Thirty patients of renal transplantation were divided into 2 groups. One group of 15 received 2 dosages of induction therapy of Zenapax and another 15 regular immunosuppressive therapy. IL-2, IL-10, STAT5 and CD40L were tested followed up at 2 hours pre- transplantation, 1, 3 and 6 months post-transplantation. Results The levels of IL-2 and STAT had no difference between the induction group and the control group. The level of IL-10 of induction group(59. 4 ± 7.7 ) ng/L was obviously higher than control group ( 36. 8 ± 8.4 ) ng/L at 3 months post-transplantation. CD40L level of induction group ( 10. 6 ± 3.6 ) was lower than control group ( 35.6 ± 8. 4 ) at 1 month posttransplantation. Conclusion Zenapax can reduce B-cell-mediated humoral immunity at 1 month posttransplantation through CD40L pathway.
出处
《中华医学杂志》
CAS
CSCD
北大核心
2009年第36期2565-2567,共3页
National Medical Journal of China