Natural killing target antigens as inducers of interferon: studies with an immunoselected, natural killing-resistant human T lymphoblastoid cell line.
Natural killing target antigens as inducers of interferon: studies with an immunoselected, natural killing-resistant human T lymphoblastoid cell line.
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DOI：
10.4049/jimmunol.134.2.971
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发表时间：
1985-02
影响因子：
4.4
通讯作者：
D. Howell;P. Andreotti;J. Dawson;P. Cresswell
中科院分区：
文献类型：
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作者：
D. Howell;P. Andreotti;J. Dawson;P. Cresswell
通过与外周血单核细胞 (PBMC) 共培养，对人 T 类淋巴母细胞系 CEM 进行免疫选择，以抵抗自然杀伤 (NK) 细胞介导的裂解。当使用 PBMC 或贴壁细胞耗尽的 PBMC 作为效应细胞时，所得亚系 CEM.NKR 的 NK 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，其 NK 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。未标记的 CEM 在抑制标记 CEM 靶细胞的 NK 裂解方面比未标记的 CEM.NKR 有效 8 至 32 倍，并且在单细胞结合测定中，CEM 结合的 Percoll 梯度富集 LGL 比 CEM.NKR 多 1.9 至 3.9 倍，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 NK 抗性变体保持了其对 IFN-α 抗增殖作用的敏感性，表明这些现象可能是由 NK 靶结构以外的分子介导的。通过使用对白细胞抗原和转铁蛋白受体特异性的单克隆抗体进行间接免疫荧光，并通过 HLA-A 和 B 特异性的微细胞毒性分型对 CEM 和 CEM.NKR 进行比较，未发现重大差异。
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.