Autophagy promotes MHC class II presentation of peptides from intracellular source proteins
Autophagy promotes MHC class II presentation of peptides from intracellular source proteins
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DOI：
10.1073/pnas.0501190102
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发表时间：
2005-05-31
影响因子：
11.1
通讯作者：
Stevanovic, S
中科院分区：
文献类型：
--
作者：
Dengjel, J;Schoor, O;Stevanovic, S
MHC-肽复合物介导适应性免疫的关键功能。按照经典观点，MHC-I 分子呈递来自细胞内源蛋白的肽，而 MHC-II 分子呈递来自外源蛋白和膜蛋白的抗原肽。然而，已经观察到这两条途径之间存在大量串扰。我们研究了自噬对 MHC-II 配体组的影响，并证明了自噬诱导后肽呈递发生了显着改变。与来自膜和分泌蛋白的肽相比，MHC-II 上来自细胞内和溶酶体源蛋白的肽的呈递强烈增加。此外，自噬影响 MHC-II 抗原加工机制。我们的研究阐明了自噬对 II 类肽库的深远影响，并表明这一发现对 CD4(+) T 细胞介导的过程的调节具有影响。
MHC-peptide complexes mediate key functions in adaptive immunity. in a classical view, MHC-I molecules present peptides from intracellular source proteins, whereas MHC-II molecules present antigenic peptides from exogenous and membrane proteins. Nevertheless, substantial crosstalk between these two pathways has been observed. We investigated the influence of autophagy on the MHC-II ligandome and demonstrated that peptide presentation is altered considerably upon induction of autophagy. The presentation of peptides from intracellular and lysosomal source proteins was strongly increased on MHC-II in contrast with peptides from membrane and secreted proteins. In addition, autophagy influenced the MHC-II antigen-processing machinery. Our study illustrates a profound influence of autophagy on the class II peptide repertoire and suggests that this finding has implications for the regulation of CD4(+) T cell-mediated processes.