CD8+T cell specificity depends on the recognition of MHC class I–epitope complexes at the cell surface. These epitopes are mainly produced via degradation of proteins by the proteasome, generating fragments of the original sequence. However, it is now clear that proteasomes can produce a significant portion of epitopes by reshuffling the antigen sequence, thus expanding the potential antigenic repertoire. MHC class I-restricted spliced epitopes have been described in tumors and infections, suggesting an unpredicted relevance of these peculiar peptides. We review current knowledge about proteasome-catalyzed peptide splicing (PCPS), the emerging rules governing this process, and the potential implications for our understanding and therapeutic use of CD8+T cells, as well as mechanisms generating other non-canonical antigenic epitopes targeted by the T cell response.

中文翻译：

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翻译后肽剪接和T细胞反应

CD8 + T细胞的特异性取决于在细胞表面对I类MHC表位复合物的识别。这些表位主要是通过蛋白酶体降解蛋白质，产生原始序列的片段而产生的。然而，现在清楚的是，蛋白酶体可以通过改组抗原序列而产生很大一部分的表位，从而扩展了潜在的抗原库。已经在肿瘤和感染中描述了MHC I类限制性剪接表位，表明这些特殊肽的不可预测的相关性。我们回顾了有关蛋白酶体催化的肽剪接（PCPS）的最新知识，控制该过程的新兴规则以及对我们理解和治疗CD8 + T细胞的潜在影响，