Rehm Armin, Engelsberg Arne, Tortorella Domenico, Körner Ida J, Lehmann Insa, Ploegh Hidde L, Höpken Uta E
Robert-Rössle-Klinik, Department of Hematology, Oncology and Tumorimmunology, Universitätsklinikum Charite, Max Delbrück Center for Molecular Medicine, Berlin, Germany.
J Virol. 2002 May;76(10):5043-50. doi: 10.1128/jvi.76.10.5043-5050.2002.
Human cytomegalovirus (HCMV) encodes several proteins that inhibit major histocompatibility complex (MHC) class I-dependent antigen presentation. The HCMV products US2 and US11 are each sufficient for causing the dislocation of human and murine MHC class I heavy chains from the lumen of the endoplasmic reticulum to the cytosol, where the heavy chains are readily degraded. The apparent redundancy of US2 and US11 has been probed predominantly in cultured cell lines, where differences in their specificities were shown for murine and human MHC class I locus products. Here, we expressed US11 and US2 via adenovirus vectors and show that US11 exhibits a superior ability to degrade MHC class I molecules in primary human dendritic cells. MHC class II complexes are unaffected by US2- and US11-mediated attack. We suggest that multiple HCMV-encoded immunoevasions have evolved complementary functions in response to diverse host cell types and tissues.
人巨细胞病毒（HCMV）编码多种蛋白，这些蛋白可抑制主要组织相容性复合体（MHC）I类依赖性抗原呈递。HCMV产物US2和US11各自足以使人和鼠MHC I类重链从内质网腔移位至胞质溶胶，在胞质溶胶中重链易于降解。US2和US11明显的冗余性主要在培养细胞系中进行了探究，在这些细胞系中，已显示出它们对鼠和人MHC I类基因座产物的特异性存在差异。在此，我们通过腺病毒载体表达US11和US2，并表明US11在原代人树突状细胞中具有更强的降解MHC I类分子的能力。MHC II类复合体不受US2和US11介导攻击的影响。我们认为，多种HCMV编码的免疫逃避蛋白已进化出互补功能，以应对不同的宿主细胞类型和组织。
