Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2019 Sep:113:2-5.
doi: 10.1016/j.molimm.2017.10.021. Epub 2017 Nov 8.

Role of autophagy in MHC class I-restricted antigen presentation

Affiliations
Review

Role of autophagy in MHC class I-restricted antigen presentation

Luc Van Kaer et al. Mol Immunol. 2019 Sep.

Abstract

Major histocompatibility complex (MHC) class I molecules present peptide antigens to MHC class I-restricted CD8+ T lymphocytes. The peptides loaded onto MHC class I molecules are typically derived from cytosolic antigens, which includes both self and foreign proteins. In addition to this classical MHC class I antigen presentation pathway, some cell types, especially dendritic cells can present antigens from exogenous sources to MHC class I-restricted CD8+ T cells, in a process called cross-presentation. A variety of cellular processes, including endocytosis, vesicle trafficking, and autophagy, play critical roles in these antigen presentation pathways. In this review article, we discuss the role of autophagy, an intracellular degradation system that delivers cytoplasmic constituents to lysosomes, in MHC class I-restricted antigen presentation. A mechanistic understanding of the role of autophagy-related proteins in MHC class I restricted antigen presentation may guide future efforts in manipulating autophagy to prevent or treat human disease.

Keywords: Antigen presentation; Autophagy; Autophagy-related proteins; CD8(+) T cells; MHC class I; Vps34.

PubMed Disclaimer

Conflict of interest statement

Conflict of Interest

The authors have no conflict of interest to disclose.

Similar articles

Cited by

References

    1. Backer JM. The intricate regulation and complex functions of the class III phosphoinositide 3-kinase Vps34. Biochem J. 2016;473:2251–2271. - PubMed
    1. Baghdadi M, et al. TIM-4 glycoprotein-mediated degradation of dying tumor cells by autophagy leads to reduced antigen presentation and increased immune tolerance. Immunity. 2013;39:1070–1081. - PubMed
    1. Bevan MJ. Cross-priming. Nat Immunol. 2006;7:363–365. - PubMed
    1. Blum JS, et al. Pathways of antigen processing. Annu Rev Immunol. 2013;31:443–473. - PMC - PubMed
    1. Cruz FM, et al. The biology and underlying mechanisms of cross-presentation of exogenous antigens on MHC-I molecules. Annu Rev Immunol. 2017;35:149–176. - PMC - PubMed

Publication types

MeSH terms

Substances