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Journal article

ATGs help MHC class II, but inhibit MHC class I antigen presentation.

  • Loi M a Viral Immunobiology , Institute of Experimental Immunology, University of Zurich , Zurich , Switzerland.
  • Gannagé M b Department of Pathology and Immunology , School of Medicine, University of Geneva , Geneva , Switzerland.
  • Münz C a Viral Immunobiology , Institute of Experimental Immunology, University of Zurich , Zurich , Switzerland.
  • 2016-07-22
Published in:
  • Autophagy. - 2016
AAK1
Atg8/LC3
LC3-associated phagocytosis
influenza virus
intracellular antigen processing
Animals
Antigen Presentation
Autophagy
Autophagy-Related Protein 5
Autophagy-Related Protein 7
CD8-Positive T-Lymphocytes
Cell Membrane
Cell-Free System
Dendritic Cells
Histocompatibility Antigens Class II
Humans
Macrophages
Phagocytosis
T-Lymphocytes
English 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.
Language
  • English
Open access status
bronze
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Persistent URL
https://susi.usi.ch/global/documents/226538
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