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Immunity. 2014 Mar 20;40(3):389-99. doi: 10.1016/j.immuni.2013.12.015. Epub 2014 Mar 13.

Clec12a is an inhibitory receptor for uric acid crystals that regulates inflammation in response to cell death.

Author information

  • 1Institut für Klinische Chemie und Pathobiochemie, Klinikum rechts der Isar, Technische Universität München, 81675 Munich, Germany.
  • 2Lehrstuhl für Proteomik und Bioanalytik, Technische Universität München, Emil Erlenmeyer Forum 5, 85354 Freising, Germany.
  • 3Medizinische Klinik und Poliklinik IV, Klinikum der Universität München (LMU), 80336 München, Germany.
  • 4Institut für Medizinische Mikrobiologie, Immunologie und Hygiene, Technische Universität München, 81675 Munich, Germany.
  • 5Max Planck Institute of Molecular Cell Biology and Genetics, 01307 Dresden, Germany.
  • 6Institut für Klinische Chemie und Pathobiochemie, Klinikum rechts der Isar, Technische Universität München, 81675 Munich, Germany. Electronic address: jruland@lrz.tum.de.

Abstract

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.

Copyright © 2014 Elsevier Inc. All rights reserved.

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PMID:
24631154
[PubMed - indexed for MEDLINE]
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