联合免疫抑制剂对肾移植患者血淋巴细胞表面淋巴细胞功能相关抗原-1和L-选择素表达的影响

Influence of combined immunosuppressants on CD62L, CD11a expression of lymphocytes from peripheral blood in renal allograft recipients and Implication

目的 探讨联合免疫抑制剂对肾移植受者外周血淋巴细胞表面淋巴细胞功能相关抗原 1(CD11a)和L 选择素 (CD6 2L)表达的作用。方法 利用单克隆抗体 流式细胞仪荧光免疫技术 ,动态观察 10例肾移植稳定病人 (稳定组 )和 10例排斥反应病人 (排斥组 )淋巴细胞CD6 2L、CD11a表达 ;急性期及排斥反应时予甲基波尼松龙 (MP) ,早期辅以抗胸腺淋巴细胞球蛋白 (ATG)。结果 稳定组应用免疫抑制剂后CD11a表达降低 ,第 9d最明显 [(2 2 .9± 8.9) % ,P <0 .0 1],停用ATG后回升 ,但仍明显低于术前组 ,CD6 2L与术前组差异无显著性 (P >0 .0 5 )。排斥组 5～ 7d排斥反应时二者表达均明显升高 ,给予MP后CD11a迅速下降 ,而CD6 2L无变化。结论 联合免疫抑制剂能明显抑制CD11a抗原表达 ;ATG对协同CD11a低水平表达和诱导免疫耐受起重要作用。

Objective\ To investigate the influence of combined immunosuppressants on CD62L and CD11a expression of lymphocytes from peripheral blood in renal allograft recipients and implication. Methods\ The dynamic changes in CD62L and CD11a levels in lymphocytes in different time points were examined by using mAb FACS immunofluorescence technique in 10 renal allograft recipients in stable course (stable group) and 10 with acute rejection (rejection group) after operation. The recipients were subjected to triple drug therapy and methylprednisolone (MP) was used for anti rejection treatment and in acute stage and antithymocyte lymphocyte globulin (ATG) was introduced simultaneously in the early stage (within 10 days). Results\ The expression of CD11a in lymphocytes was increased after administration of immunosuppressants in stable group, reaching the peak at 9th day [(22.9±8.9), P <0.01], and returned after stopping ATG, but significantly lower than in the preoperative group. No significant difference in CD62L between the suppressants treated group and preoperative groups was found. In rejection group, both CD62L and CD11a expression was obviously increased at the 5th to 7th day of rejection, and CD11a was rapidly decreased, but CD62L showed no change.Conclusion\ The immunosuppressants (especially MP) can suppress the expression of CD11a in lymphocytes evidently. ATG may play an important role in maintaining lower level of CD11a and inducing the immunologic tolerance.