ATGs help MHC class II, but inhibit MHC class I antigen presentation. Issue 9 (1st September 2016)

• Record Type: Journal Article
• Authors: Loi, Monica; Gannagé, Monique; Münz, Christian
• Is Part Of: Autophagy. Volume 12:Issue 9(2016)
• Page Start: 1681
• Page End: 1682
• Publication Date: 2016-09-01
• Subjects: AAK1 -- Atg8/LC3 -- influenza virus -- intracellular antigen processing -- LC3-associated phagocytosis; Autophagic vacuoles -- Periodicals; Apoptosis -- Periodicals; Cell death -- Periodicals; Lysosomes -- Periodicals; Degeneration (Pathology) -- Periodicals; Autophagy -- Periodicals; Cell Death -- Periodicals; Lysosomes -- Periodicals; Periodicals; 571.936
• DOI: 10.1080/15548627.2016.1203488
• Languages: English
• ISSNs: 1554-8627

Abstract

ABSTRACT: We have recently shown that the LC3/Atg8 lipidation machinery of macroautophagy is involved in the internalization of MHC class I molecules. Decreased internalization in the absence of ATG5 or ATG7 leads to MHC class I surface stabilization on dendritic cells and macrophages, resulting in elevated CD8 + T cell responses during viral infections and improved immune control. Here, we discuss how the autophagic machinery supports MHC class II restricted antigen presentation, while compromising MHC class I presentation via internalization and degradation.