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Cited by 264

The DOI matches its Crossref record; 150 of the 150 references it cites were found in a registry or an index.

Enhancing Immunity Through Autophagy

Münz, Christian·2009·Annual Review of Immunology

Abstract

Next to the proteasome, autophagy is the main catabolic pathway for the degradation of cytoplasmic constituents. The immune system uses it both as an effector mechanism to clear intracellular pathogens and as a mechanism to monitor its products for evidence of pathogen invasion and cellular transformation. Because autophagy delivers intracellular material for lysosomal degradation, its products are primarily loaded onto MHC class II molecules and are able to stimulate CD4+ T cells. This process might shape the self-tolerance of the CD4+ T cell repertoire and stimulate CD4+ T cell responses against pathogens and tumors. Beyond antigen processing, autophagy's role in cell survival is to assist the clonal expansion of B and T cells for efficient adaptive immune responses. These immune-enhancing functions make autophagy an attractive target for therapeutic manipulation in human disease.

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Crossref · 10.1146/annurev.immunol.021908.132537

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Metadata

Authors
Münz, C.
Venue
Annual Review of Immunology
Published
2009-04-01
Volume
27
Issue
1
Pages
423-449
ISSN
  • 0732-0582 (ISSN-L)
  • 1545-3278
OpenAlex
W2112523199
Cited by
264
References
150
FWCI
2.73
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Enhancing Immunity Through Autophagy. https://app.cochat.ai/papers/10.1146/annurev.immunol.021908.132537
The paper
Münz, C. (2009). Enhancing Immunity Through Autophagy. Annual Review of Immunology. https://doi.org/10.1146/annurev.immunol.021908.132537

Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.