Instituto de Salud Carlos III, Centro Nacional de Microbiología, 28220 Majadahonda (Madrid), Spain and.
Unité d'Immunité Cellulaire Antivirale, Département d'Immunologie, Institut Pasteur, Paris Cedex 15, France.
J Biol Chem. 2012 Mar 23;287(13):9990-10000. doi: 10.1074/jbc.M111.314856. Epub 2012 Feb 1.
The transporter associated with antigen processing (TAP) translocates the viral proteolytic peptides generated by the proteasome and other proteases in the cytosol to the endoplasmic reticulum lumen. There, they complex with nascent human leukocyte antigen (HLA) class I molecules, which are subsequently recognized by the CD8(+) lymphocyte cellular response. However, individuals with nonfunctional TAP complexes or tumor or infected cells with blocked TAP molecules are able to present HLA class I ligands generated by TAP-independent processing pathways. Herein, using a TAP-independent polyclonal vaccinia virus-polyspecific CD8(+) T cell line, two conserved vaccinia-derived TAP-independent HLA-B*0702 epitopes were identified. The presentation of these epitopes in normal cells occurs via complex antigen-processing pathways involving the proteasome and/or different subsets of metalloproteinases (amino-, carboxy-, and endoproteases), which were blocked in infected cells with specific chemical inhibitors. These data support the hypothesis that the abundant cellular proteolytic systems contribute to the supply of peptides recognized by the antiviral cellular immune response, thereby facilitating immunosurveillance. These data may explain why TAP-deficient individuals live normal life spans without any increased susceptibility to viral infections.
抗原加工相关转运体(TAP)将蛋白酶体和细胞质中其他蛋白酶生成的病毒蛋白水解肽转运到内质网腔。在那里,它们与新生的人类白细胞抗原(HLA)I 类分子结合,随后被 CD8(+)淋巴细胞细胞反应识别。然而,具有功能失调的 TAP 复合物的个体或肿瘤或被阻断 TAP 分子的感染细胞能够呈现由 TAP 非依赖性加工途径生成的 HLA I 类配体。在此,使用 TAP 非依赖性多克隆痘苗病毒-多特异性 CD8(+)T 细胞系,鉴定了两个保守的痘苗衍生的 TAP 非依赖性 HLA-B*0702 表位。这些表位在正常细胞中的呈递通过涉及蛋白酶体和/或不同金属蛋白酶(氨基、羧基和内肽酶)亚群的复杂抗原加工途径发生,在被特异性化学抑制剂感染的细胞中,这些途径被阻断。这些数据支持这样一种假设,即丰富的细胞蛋白水解系统有助于提供抗病毒细胞免疫反应识别的肽,从而促进免疫监视。这些数据可以解释为什么 TAP 缺陷个体能够正常生活而不会增加对病毒感染的易感性。