Porcine aortic endothelial cells transfected with HLA-G are partially protected from xenogeneic human NK cytotoxicity

Porcine aortic endothelial cells transfected with HLA-G are partially protected from xenogeneic human NK cytotoxicity
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DOI:
10.1016/s0198-8859(00)00202-0
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发表时间:
2000-11-01
期刊:
影响因子:
2.7
通讯作者:
Seebach, JD
Seebach, JD
中科院分区:
医学4区
文献类型:
--
作者:
Forte, P;Matter-Reissmann, UB;Seebach, JD

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在这项研究中,我们测试了 HLA-G 的表达是否可以保护猪内皮细胞 (PEC) 免受人类自然杀伤 (NK) 细胞介导的裂解。由于 HLA-E 不存在于 PEG 中,因此该模型为研究 HLA-G 在 NK 抑制中的直接作用提供了理想的工具。用编码 HLA-G1 蛋白的载体稳定转染永生化猪主动脉内皮细胞 (PED),并通过行细胞计数分析证明表面表达。尽管 HLA-G 不会损害人类 NK 细胞与 FED 的粘附,但 HLA-G 的表达部分保护 FED 免受来自不同供体的多克隆 NK 系介导的裂解。 A decrease of the surface-expression of HLA-G on FED corresponded to a loss of the capacity of FED to inhibit NK cytotoxicity, indicating chat the surface density of HLA-G molecules must exceed a certain threshold to protect target cells.总之,这些数据表明 HLA-G 独立于 HLA-E 的存在,只能部分且低效地保护 FED 免受人类 NE 的影响;细胞介导的细胞毒性。因为ILT-2/LIR-1表达与HLA-G介导的抑制无关,我们推测外周血NK细胞表达的其他尚未鉴定的受体参与HLA-G的识别。 (C) 美国组织相容性和免疫遗传学学会,2000 年。由 Elsevier Science Inc. 出版。
In this study we tested whether the expression of HLA-G protects porcine endothelial cells (PEC) from the lysis mediated by human natural killer (NK) cells. Because HLA-E is nor: present in PEG, this model provides an ideal tool to study the direct role of HLA-G in NK inhibition. Immortalized porcine aortic endothelial cells (PED) were stably transfected with a vector coding for the HLA-G1 protein and surface expression was demonstrated by Row cytometry analysis. Although the adhesion of human NK cells to FED was not compromised by HLA-G, the expression of HLA-G partially protected FED from the lysis mediated by polyclonal NK lines derived from different donors. A decrease of the surface-expression of HLA-G on FED corresponded to a loss of the capacity of FED to inhibit NK cytotoxicity, indicating chat the surface density of HLA-G molecules must exceed a certain threshold to protect target cells. In summary, these data show that HLA-G, independent from the presence of HLA-E, can only partially and inefficiently protect FED from human NE; cell-mediated cytotoxicity. Because ILT-2/LIR-1 expression did not correlate with HLA-G mediated inhibit ion, we hypothesize that other yet unidentified receptors expressed by peripheral blood NK cells are involved in the recognition of HLA-G. (C) American Society for Histocompatibility and Immunogenetics, 2000. Published by Elsevier Science Inc.