期刊
IMMUNITY
卷 40, 期 3, 页码 389-399出版社
CELL PRESS
DOI: 10.1016/j.immuni.2013.12.015
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资金
- Bavarian Ministry of Sciences, Research and the Arts in the Framework of the Bavarian Molecular Biosystems Research Network
- SFB grants from Deutsche Forschungsgemeinschaft
- ERC
Recognition of cell death by the innate immune system triggers inflammatory responses. However, how these reactions are regulated is not well understood. Here, we identify the inhibitory C-type lectin receptor Clec12a as a specific receptor for dead cells. Both human and mouse Clec12a could physically sense uric acid crystals (monosodium urate, MSU), which are key danger signals for cell-death-induced immunity. Clec12a inhibited inflammatory responses to MSU in vitro, and Clec12a-deficient mice exhibited hyperinflammatory responses after being challenged with MSU or necrotic cells and after radiation-induced thymocyte killing in vivo. Thus, we identified a negative regulatory MSU receptor that controls noninfectious inflammation in response to cell death that has implications for autoimmunity and inflammatory disease.
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