期刊
CELL REPORTS
卷 15, 期 8, 页码 1757-1770出版社
CELL PRESS
DOI: 10.1016/j.celrep.2016.04.053
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资金
- Ministry of Education, Taiwan
- European Federation of Immunological Societies (EFIS)
- German Research Foundation [FOR 2372]
- Ministry of Science and Technology, Taiwan [MOST101-2320-B-182-029-MY3, MOST104-2320-B-182-035-MY3]
- Chang Gung Memorial Hospital [CMRPD1A0181-3, CMRPD1D0072-3, CMRPD1D0391-2]
- Thyssen Foundation [2015-00387]
- Tenovus Cancer Care [PHD2009/L15] Funding Source: researchfish
Natural killer (NK) cells possess potent cytotoxic mechanisms that need to be tightly controlled. Here, we explored the regulation and function of GPR56/ADGRG1, an adhesion G protein-coupled receptor implicated in developmental processes and expressed distinctively in mature NK cells. Expression of GPR56 was triggered by Hobit (a homolog of Blimp-1 in T cells) and declined upon cell activation. Through studying NK cells from polymicrogyria patients with disease-causing mutations in ADGRG1, encoding GPR56, and NK-92 cells ectopically expressing the receptor, we found that GPR56 negatively regulates immediate effector functions, including production of inflammatory cytokines and cytolytic proteins, degranulation, and target cell killing. GPR56 pursues this activity by associating with the tetraspanin CD81. We conclude that GPR56 inhibits natural cytotoxicity of human NK cells.
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