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Related Experiment Video

Updated: Jan 31, 2026

Immunopeptidomics: Isolation of Mouse and Human MHC Class I- and II-Associated Peptides for Mass Spectrometry Analysis

Immunopeptidomics: Isolation of Mouse and Human MHC Class I- and II-Associated Peptides for Mass Spectrometry Analysis

Published on: October 15, 2021

MHC Class I Internalization via Autophagy Proteins.

Monica Loi¹, Laure-Anne Ligeon¹, Christian Münz²

¹Viral Immunobiology, Institute of Experimental Immunology, University of Zürich, Zürich, Switzerland.

Methods in Molecular Biology (Clifton, N.J.)

|January 6, 2019

Summary

Macroautophagy regulates MHC class I surface levels by controlling internalization via AAK1. Macroautophagy deficiency stabilizes MHC class I, enhancing CD8+ T cell priming and reducing pathology during influenza infection.

Keywords:

Atg5 Atg7 Autophagy Dendritic cells MHC class I

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Last Updated: Jan 31, 2026

Immunopeptidomics: Isolation of Mouse and Human MHC Class I- and II-Associated Peptides for Mass Spectrometry Analysis

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Published on: October 15, 2021

Visualizing Antigen Specific CD4+ T Cells using MHC Class II Tetramers

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Study of Protein-protein Interactions in Autophagy Research

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Published on: September 9, 2017

Area of Science:

Immunology
Cell Biology
Molecular Biology

Background:

Macroautophagy is a key cellular process involved in immunity.
It delivers antigens for MHC class II presentation.
Its role in MHC class I antigen presentation is less understood.

Purpose of the Study:

To investigate the role of macroautophagy in MHC class I trafficking and CD8+ T cell priming.
To characterize the impact of macroautophagy deficiency on MHC class I surface levels.

Main Methods:

Monitoring MHC class I internalization in dendritic cells lacking macroautophagy components.
Characterizing interactions between MHC class I/Atg8/LC3 and AAK1.
Evaluating influenza A-specific CD8+ T cell responses in mice with depleted Atg5 in dendritic cells.

Main Results:

Macroautophagy deficiency stabilizes MHC class I molecules on the surface of antigen-presenting cells.
This stabilization results from defective MHC class I internalization mediated by AAK1 and clathrin-mediated endocytosis.
Macroautophagy-dependent MHC class I stabilization enhances CD8+ T cell priming during influenza A infection, reducing pathology.

Conclusions:

Macroautophagy machinery regulates MHC class I surface levels through control of internalization.
This pathway is crucial for effective CD8+ T cell priming and immune response against viral infections.