期刊
ANNUAL REVIEW OF IMMUNOLOGY
卷 27, 期 -, 页码 423-449出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev.immunol.021908.132537
关键词
innate immunity; immune escape; MHC class II; T cell survival; tolerance
类别
资金
- Dana Foundation's Neuroimmunology
- Arnold and Mabel Beckman Foundation
- Alexandrine and Alexander Sinsheimer Foundation
- Burroughs Wellcome Fund
- Starr Foundation
- National Cancer Institute [R01CA108609, R01CA101741]
- National Institute of Allergy and Infectious Diseases [RFP-NIH-NIAID-DAIDS-BAA-06-19]
- Foundation for the National Institutes of Health
- Institutional Clinical and Translational Science Award
- NATIONAL CANCER INSTITUTE [R01CA101741, R01CA108609] Funding Source: NIH RePORTER
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 IT 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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