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本研究的目的是探讨造血干细胞移植后杀伤细胞抑制性受体 (KIR)CD15 8和CD94与GVHD发生的关系。用流式细胞术检测分析T淋巴细胞和NK细胞表达CD15 8a,CD15 8b和CD94表达状况 ,同时用PCR方法分析供受者HLA Cw配型 ,比较异基因外周血造血干细胞移植 (allo PBSCT)和脐血移植 (UCBT)后该KIR分子变化和HLA Cw相合或错配与GVHD发生的关系。结果表明 :无论是PBSCT或是UCBT ,移植后CD3+CD15 8a+和CD3+CD15 8b+T细胞均增高并以CD8+CD15 8b+细胞升高为主。发生急性与慢性GVHD组CD3+CD15 8b+细胞均呈不同程度升高 ,在急性GVHD病例中升高最明显。急性GVHD期 (即移植早期 )KIR表达增高 ,慢性GVHD阶段 (即移植后期 )KIR呈减低趋势。CD94主要表达于CD3+CD8+T细胞 ,在UCBT或PBSCT后CD94在CD4 +T细胞和CD8+T细胞均明显增高。 5例HLA Cw相合者无 1例发生重症GVHD ;2例HLA Cw不相合病例 ,有 1例发生急重症GVHD ,并死于间质性肺炎 (IP) ,另 1例为AML(M5) ,完全植入 ,无重度GVHD发生 ,但于 5 3天后复发。 4例相关相合移植中 2例无急性GVHD ,而无关相合者 4例均发生不同程度GVHD。结论 :GVHD的发生与KIR表达有一定关系。CD15 8b分子可能是移植后早期T淋巴细胞活化的负调控分子。从T细胞表达KIR来理解GVHD发生机理 ,特别是与HLA
The purpose of this study was to investigate the relationship between KIR CD15 8 and CD94 and GVHD after hematopoietic stem cell transplantation. The expression of CD15 8a, CD15 8b and CD94 in T lymphocytes and NK cells were detected by flow cytometry. Meanwhile, HLA Cw pattern was analyzed by PCR, and allogeneic peripheral blood hematopoietic stem cell transplantation (allo PBSCT) and The relationship between KIR molecular changes and HLA Cw mismatch and the occurrence of GVHD after cord blood transplantation (UCBT). The results showed that both CD3 + CD15 8a + and CD3 + CD15 8b + T cells after transplantation were elevated and CD8 + CD15 8b + cells were elevated mainly in both PBSCT and UCBT. In acute and chronic GVHD group, CD3 + CD15 8b + cells showed different degrees of elevation, and the most obvious increase in acute GVHD cases. The expression of KIR increased in acute GVHD (early stage of transplantation) and decreased in chronic stage of GVHD (late transplantation). CD94 mainly expressed in CD3 + CD8 + T cells, CD94 in CD4 + T cells and CD8 + T cells were significantly increased after UCBT or PBSCT. None of the 5 HLA Cw matched patients had severe GVHD; 2 had HLA Cw mismatch cases, 1 had severe GVHD and died of interstitial pneumonia (IP), and the other had AML (M5) completely Implantation, no severe GVHD occurred but relapsed after 53 days. There were no acute GVHD in 4 cases of related co-transplantation, and 4 cases of unrelated GVHD. Conclusion: The occurrence of GVHD is related to the expression of KIR. The CD158b molecule may be a negative regulator of early T lymphocyte activation after transplantation. KIR expression from T cells to understand the pathogenesis of GVHD, especially with HLA