Inhibition of natural killer cell-mediated cytotoxicity by kaposi's sarcoma-associated herpesvirus K5 protein
Inhibition of natural killer cell-mediated cytotoxicity by kaposi's sarcoma-associated herpesvirus K5 protein
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DOI：
10.1016/s1074-7613(00)00036-4
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发表时间：
2000-09-01
期刊：
影响因子：
32.4
通讯作者：
Jung, JU
中科院分区：
文献类型：
--
作者：
Ishido, S;Choi, JK;Jung, JU
卡波西肉瘤相关疱疹病毒 (KSHV) K3 和 K5 蛋白显着下调 MHC I 类分子。然而，尽管 MHC I 类下调可能保护 KSHV 感染的细胞免受细胞毒性 T 淋巴细胞识别，但这些细胞成为自然杀伤 (NK) 细胞介导的裂解的潜在目标。我们现在证明 K5 还下调 ICAM-1 和 B7-2，它们是 NK 细胞介导的细胞毒性受体的配体。因此，K5 表达可显着抑制 NK 细胞介导的细胞毒性。相反，B7-2 和 ICAM-1 的从头表达使 W 表达细胞对 NK 细胞介导的细胞毒性重新敏感。这是一种新型病毒免疫逃避策略，KSHV K5 通过下调 NK 细胞介导的细胞毒性受体的细胞配体来实现免疫逃避。
Kaposi's sarcoma-associated herpesvirus (KSHV) K3 and K5 proteins dramatically downregulate MHC class I molecules. However, although MHC class I downregulation may protect KSHV-infected cells from cytotoxic T lymphocyte recognition, these cells become potential targets for natural killer (NK) cell-mediated lysis. We now show that K5 also downregulates ICAM-1 and B7-2, which are ligands for NK cell-mediated cytotoxicity receptors. As a consequence, K5 expression drastically inhibits NK cell-mediated cytotoxicity. Conversely, de novo expression of B7-2 and ICAM-1 resensitizes the W-expressing cells to NK cell-mediated cytotoxicity. This is a novel viral immune evasion strategy where KSHV K5 achieves immune avoidance by downregulation of cellular ligands for NK cell-mediated cytotoxicity receptors.