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Autophagy beyond intracellular MHC Class II antigen presentation


Münz, Christian (2016). Autophagy beyond intracellular MHC Class II antigen presentation. Trends in Immunology, 37(11):755-763.

Abstract

Autophagy is a group of cellular pathways that deliver cytoplasmic constituents for lysosomal degradation. The peptides generated from these pathways can be presented by MHC II molecules, making autophagy an important source of antigens for CD4+ T cells. In addition, modules of the molecular machinery of autophagy were found in recent years to also influence extracellular antigen processing for MHC Class I and Class II presentation, as well as regulation of MHC Class I surface expression. These studies paint a more complicated picture of how regulation of individual autophagy proteins influences adaptive immunity. The respective pathways, especially in regard to their net outcome for CD4+ helper and CD8+ cytotoxic T cell responses in vivo, will be discussed in this review.

Abstract

Autophagy is a group of cellular pathways that deliver cytoplasmic constituents for lysosomal degradation. The peptides generated from these pathways can be presented by MHC II molecules, making autophagy an important source of antigens for CD4+ T cells. In addition, modules of the molecular machinery of autophagy were found in recent years to also influence extracellular antigen processing for MHC Class I and Class II presentation, as well as regulation of MHC Class I surface expression. These studies paint a more complicated picture of how regulation of individual autophagy proteins influences adaptive immunity. The respective pathways, especially in regard to their net outcome for CD4+ helper and CD8+ cytotoxic T cell responses in vivo, will be discussed in this review.

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Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > Institute of Experimental Immunology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:2016
Deposited On:16 Jan 2017 10:50
Last Modified:02 Feb 2018 11:34
Publisher:Elsevier
ISSN:1471-4906
OA Status:Closed
Publisher DOI:https://doi.org/10.1016/j.it.2016.08.017
PubMed ID:27667710

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