Endocytosis regulation by autophagy proteins in MHC restricted antigen presentation. (June 2018)

• Record Type: Journal Article
• Authors: .Keller, Christian W; Loi, Monica; Ligeon, Laure-Anne; Gannagé, Monique; Lünemann, Jan D; Münz, Christian
• Is Part Of: Current opinion in immunology. Volume 52(2018)
• Page Start: 68
• Page End: 73
• Publication Date: 2018-06
• Subjects: Immunology -- Periodicals; Allergy -- Periodicals; Immunology -- Abstracts -- Periodicals; Allergy -- Abstracts -- Periodicals; 616.079
• DOI: 10.1016/j.coi.2018.04.014
• Languages: English
• ISSNs: 0952-7915

Abstract

Highlights: LC3 associated phagocytosis supports extracellular MHC class II antigen processing. LC3 lipidation facilitates classical and non-classical MHC class I internalization. LC3 assisted endocytosis compromises intracellular MHC class I antigen presentation. Abstract : The macroautophagy machinery supports membrane remodeling and fusion events that lead to the engulfment of cytoplasmic constituents in autophagosomes and their degradation in lysosomes. The capacity of this machinery to regulate membrane adaptors and influence vesicle fusion with lysosomes seems to be used not only for autophagosomes, but also for endosomes. We summarize recent evidence that two aspects of endocytosis are regulated by parts of the macroautophagy machinery. These are recruitment of adaptors for the internalization of surface receptors and the fusion of phagosomes with lysosomes. Antigen processing for MHC presentation is affected by these alternative functions of the macroautophagy machinery. Primarily extracellular antigen presentation by MHC class II molecules after phagocytosis benefits from this regulation of phagosome maturation. Furthermore, MHC class I molecules are more efficiently internalized in the presence of the core macroautophagy machinery. The identification of these alternative functions of macroautophagy proteins not only complicates the interpretation of their deficiencies in biological processes, but could also be harnessed for the regulation of antigen presentation to T cells.