期刊
ANNUAL REVIEW OF IMMUNOLOGY, VOL 31
卷 31, 期 -, 页码 413-441出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev-immunol-032712-095951
关键词
natural killer cells; innate immunity; MICA; ULBP; RAE-1; MULT1
类别
资金
- National Institutes of Health [RO1AI039642, RO1CA093678]
- Prostate Cancer Foundation
- Biomedical Research Council [07/1/21/19/513]
- National Research Foundation
- Cancer Research Institute Postdoctoral Fellowship
- Samsung Scholarship Foundation
- National Science Foundation Predoctoral Fellowship
- NATIONAL CANCER INSTITUTE [R01CA093678] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI039642] Funding Source: NIH RePORTER
NKG2D is an activating receptor expressed by all NK cells and subsets of T cells. It serves as a major recognition receptor for detection and elimination of transformed and infected cells and participates in the genesis of several inflammatory diseases. The ligands for NKG2D are self-proteins that are induced by pathways that are active in certain pathophysiological states. NKG2D ligands are regulated transcriptionally, at the level of mRNA and protein stability, and by cleavage from the cell surface. In some cases, ligand induction can be attributed to pathways that are activated specifically in cancer cells or infected cells. We review the numerous pathways that have been implicated in the regulation of NKG2D ligands, discuss the pathologic states in which those pathways are likely to act, and attempt to synthesize the findings into general schemes of NKG2D ligand regulation in NK cell responses to cancer and infection.
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