title: ATGs help MHC class II, but inhibit MHC class I antigen presentation.
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.
authors.affiliation: a Viral Immunobiology , Institute of Experimental Immunology, University of Zurich , Zurich , Switzerland.
authors.forename: Monica
authors.initials: M
authors.lastname: Loi
authors.affiliation: b Department of Pathology and Immunology , School of Medicine, University of Geneva , Geneva , Switzerland.
authors.forename: Monique
authors.initials: M
authors.lastname: Gannagé
authors.affiliation: a Viral Immunobiology , Institute of Experimental Immunology, University of Zurich , Zurich , Switzerland.
authors.forename: Christian
authors.initials: C
authors.lastname: Münz
mesh_terms: D000818:Animals; D017951:Antigen Presentation / Q000276:immunology*; D001343:Autophagy; D000071187:Autophagy-Related Protein 5 / Q000378:metabolism*; D000071193:Autophagy-Related Protein 7 / Q000378:metabolism*; D018414:CD8-Positive T-Lymphocytes / Q000166:cytology; D002462:Cell Membrane / Q000378:metabolism; D002474:Cell-Free System; D003713:Dendritic Cells / Q000378:metabolism; D000949:Histocompatibility Antigens Class II / Q000378:metabolism*; D006801:Humans; D008264:Macrophages / Q000378:metabolism; D010587:Phagocytosis; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: C502778:ATG5 protein, human; D000071187:Autophagy-Related Protein 5; D000949:Histocompatibility Antigens Class II; C509349:ATG7 protein, human; D000071193:Autophagy-Related Protein 7
keywords: AAK1; Atg8/LC3; LC3-associated phagocytosis; influenza virus; intracellular antigen processing