Howell D N, Andreotti P E, Dawson J R, Cresswell P
J Immunol. 1985 Feb;134(2):971-6.
The human T lymphoblastoid cell line CEM was subjected to immunoselection by co-culture with peripheral blood mononuclear cells (PBMC) for resistance to natural killer (NK) cell-mediated lysis. The NK susceptibility of the resulting subline, CEM.NKR, was 8.4 to 20.6% of that of CEM when PBMC or adherent cell-depleted PBMC were used as effector cells, and -7.1 to 12.1% of that of CEM when Percoll gradient-enriched large granular lymphocytes (LGL) were used. However, CEM and CEM.NKR exhibited comparable sensitivity to antibody-dependent cellular cytotoxicity. Unlabeled CEM was eight- to 32-fold more effective than unlabeled CEM.NKR in inhibiting the NK lysis of labeled CEM target cells, and CEM bound 1.9 to 3.9-fold more Percoll gradient-enriched LGL than CEM.NKR in single cell-binding assays, suggesting that the NK-resistant variant has lost the expression of NK target antigens. However, CEM.NKR was comparable to CEM in its ability to induce interferon (IFN)-alpha production by PBMC in vitro, and the NK-resistant variant maintained its susceptibility to the antiproliferative effects of IFN-alpha, indicating that these phenomena may be mediated by molecules other than NK target structures. Comparison of CEM and CEM.NKR by indirect immunofluorescence with monoclonal antibodies specific for leukocyte antigens and the transferrin receptor, and by microcytotoxicity typing for HLA-A and B specificities, revealed no major differences.
将人T淋巴母细胞系CEM与外周血单核细胞（PBMC）共培养，进行免疫选择以获得对自然杀伤（NK）细胞介导的裂解的抗性。当使用PBMC或去除贴壁细胞的PBMC作为效应细胞时，所得亚系CEM.NKR对NK的敏感性为CEM的8.4%至20.6%；当使用Percoll梯度富集的大颗粒淋巴细胞（LGL）时，CEM.NKR对NK的敏感性为CEM的-7.1%至12.1%。然而，CEM和CEM.NKR对抗体依赖性细胞毒性表现出相当的敏感性。在抑制标记的CEM靶细胞的NK裂解方面，未标记的CEM比未标记的CEM.NKR有效8至32倍；在单细胞结合试验中，CEM结合的Percoll梯度富集的LGL比CEM.NKR多1.9至3.9倍，这表明NK抗性变体已失去NK靶抗原的表达。然而，CEM.NKR在体外诱导PBMC产生干扰素（IFN）-α的能力与CEM相当，并且该NK抗性变体对IFN-α的抗增殖作用仍保持敏感性，这表明这些现象可能由NK靶结构以外的分子介导。用针对白细胞抗原和转铁蛋白受体的单克隆抗体通过间接免疫荧光以及对HLA-A和B特异性进行微量细胞毒性分型来比较CEM和CEM.NKR，未发现主要差异。
