Journal
CELL DEATH AND DIFFERENTIATION
Volume 16, Issue 1, Pages 79-86Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/cdd.2008.113
Keywords
autophagy; immunity; MHC, T cell
Categories
Funding
- Dana Foundation
- Irvington Institute's Human Immunology
- Institutional Clinical and Translational Science Pilot and Collaborative
- Arnold and Mabel Beckman Foundation
- Alexandrine and Alexander Sinsheimer Foundation
- National Cancer Institute [R01CA108609, R01CA101741]
- National Institutes of Health
- NATIONAL CANCER INSTITUTE [R01CA101741, R01CA108609] Funding Source: NIH RePORTER
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Autophagy is a homeostatic process that enables eukaryotic cells to deliver cytoplasmic constituents for lysosomal degradation, to recycle nutrients and to survive during starvation. In addition to these primordial functions, autophagy has emerged as a key mechanism in orchestrating innate and adaptive immune responses to intracellular pathogens. Autophagy restricts viral infections as well as replication of intracellular bacteria and parasites and delivers pathogenic determinants for TLR stimulation and for MHC class II presentation to the adaptive immune system. Apart from its role in defense against pathogens, autophagy-mediated presentation of self-antigens in the steady state could have a crucial role in the induction and maintenance of CD4(+) T-cell tolerance. This review describes the mechanisms by which the immune system utilizes autophagic degradation of cytoplasmic material to regulate adaptive immune responses.
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