期刊
JOURNAL OF IMMUNOLOGY
卷 167, 期 10, 页码 5527-5530出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.167.10.5527
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- NIDDK NIH HHS [DK 42166-11, R01 DK58727-01A1] Funding Source: Medline
Unlike primary T cells in lymph nodes, effector CD8(+) CTL in tissues do not express the costimulatory receptor CD28. We report that NKG2D, the receptor for stress-induced MICA and MICB molecules expressed in the intestine, serves as a potent costimulatory receptor for CTL freshly isolated from the human intestinal epithelium. Expression and function of NKG2D are selectively up-regulated by the cytokine IL-15, which is released by the inflamed intestinal epithelium. These findings identify a novel CTL costimulatory pathway regulated by IL-15 and suggest that tissues can fine-tune the activation of effector T cells based on the presence or absence of stress and inflammation. Uncontrolled secretion of IL-15 could lead to excessive induction of NKG2D and thus contribute to the development of autoimmune disease by facilitating the activation of autoreactive T cells.
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