MHC class I molecules on the cellular surface display peptides that either derive from endogenous proteins (self or viral), or from endocytosis of molecules, dying cells or pathogens. The conventional antigen‐processing pathway for MHC class I presentation depends on proteasome‐mediated degradation of the protein followed by transporter associated with antigen‐processing (TAP)‐mediated transport of the generated peptides into the endoplasmic reticulum (ER). Here, peptides are loaded onto MHC I molecules before transportation to the cell surface. However, several alternative mechanisms have emerged. These include TAP‐independent mechanisms, the vacuolar pathway and involvement of autophagy. Autophagy is a cell intrinsic recycling system. It also functions as a defence mechanism that removes pathogens and damaged endocytic compartments from the cytosol. Therefore, it appears likely that autophagy would intersect with the MHC class I presentation pathway to alarm CD8⁺ T cells of an ongoing intracellular infection. However, the importance of autophagy as a source of antigen for presentation on MHC I molecules remains to be defined. Here, original research papers which suggest involvement of autophagy in MHC I antigen presentation are reviewed. The antigens are from herpesvirus, cytomegalovirus and chlamydia. The studies point towards autophagy as important in MHC class I presentation of endogenous proteins during conditions of immune evasion. Because autophagy is a regulated process which is induced upon activation of, for example, pattern recognition receptors (PRRs), it will be crucial to use relevant stimulatory conditions together with primary cells when aiming to confirm the importance of autophagy in MHC class I antigen presentation in future studies.

中文翻译：

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自噬参与MHC I类抗原呈递。

细胞表面的MHC I类分子展示的肽要么来源于内源性蛋白质（自身或病毒），要么来源于分子的内吞作用，垂死的细胞或病原体。MHC I类呈递的常规抗原加工途径取决于蛋白酶体介导的蛋白质降解，然后是与抗原加工（TAP）介导的将生成的肽转运到内质网（ER）相关的转运蛋白。在此，在将肽转运到细胞表面之前将其装载到MHC I分子上。但是，出现了几种替代机制。这些包括独立于TAP的机制，液泡途径和自噬的参与。自噬是细胞固有的回收系统。它也起防御机制的作用，从细胞质中清除病原体和受损的内吞区室。因此，自噬似乎会与MHC I类呈递途径相交，从而发​​出警报CD8。⁺ T细胞正在进行细胞内感染。然而，自噬作为在MHC I分子上呈递的抗原来源的重要性仍有待确定。在这里，原始的研究论文，建议自噬参与MHC I抗原呈递进行了审查。抗原来自疱疹病毒，巨细胞病毒和衣原体。研究指出自噬在免疫逃逸条件下对内源性蛋白质的MHC I类呈递至关重要。由于自噬是一种受调控的过程，是由例如模式识别受体（PRR）激活而诱导的，因此，在确定自噬在I类MHC抗原呈递中的重要性时，将相关刺激条件与原代细胞一起使用至关重要在未来的研究中。