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Neumann, Konstantin; Castiñeiras-Vilariño, Mercedes; Höckendorf, Ulrike; Hannesschläger, Nicole; Lemeer, Simone; Kupka, Danny; Meyermann, Svenia; Lech, Maciej; Anders, Hans-Joachim; Kuster, Bernhard; Busch, Dirk H.; Gewies, Andreas; Naumann, Ronald; Groß, Olaf; Ruland, Jürgen
Immunity (Cambridge, Mass.), 03/2014, Letnik: 40, Številka: 3Journal Article
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. Display omitted •Clec12a is a receptor for dead cells•Uric acid crystals (MSU) are ligands for Clec12a•Clec12a limits the MSU-induced respiratory burst•Clec12a-deficient mice exhibit hyperinflammatory responses in vivo
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