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Updated: Jan 20, 2026

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The uric acid crystal receptor Clec12A potentiates type I interferon responses.

Kai Li1,2, Konstantin Neumann3, Vikas Duhan4

  • 1Institut für Klinische Chemie und Pathobiochemie, Klinikum rechts der Isar, Technische Universität München, 81675 Munich, Germany.

Proceedings of the National Academy of Sciences of the United States of America
|August 28, 2019
PubMed
Summary

Clec12A, a receptor sensing uric acid crystals, surprisingly amplifies type I interferon (IFN-I) responses. This discovery reveals a new link between damage-associated molecular patterns and innate immunity, impacting viral infection outcomes.

Keywords:
C-type lectin receptorClec12ALCMVTBK1-IRF3 signalingtype I interferon

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Area of Science:

  • Immunology
  • Molecular Biology
  • Infectious Diseases

Background:

  • Innate immunity detects pathogens and cellular damage for host defense.
  • Immune receptor signaling integration for tailored responses is complex.
  • Clec12A is an inhibitory C-type lectin receptor sensing cell death and uric acid crystals, limiting inflammation via Syk antagonism.

Purpose of the Study:

  • To investigate the role of Clec12A in regulating immune responses beyond its known inhibitory functions.
  • To elucidate the mechanism by which Clec12A influences type I interferon (IFN-I) production.
  • To determine the in vivo significance of Clec12A in antiviral immunity.

Main Methods:

  • In vitro and in vivo experiments using Clec12A-deficient models.
  • Analysis of retinoic acid-inducible gene I (RIG-I) signaling pathways.
  • Assessment of type I IFN production and IFN-stimulated gene induction.
  • Murine models of lymphocytic choriomeningitis virus (LCMV) infection.

Main Results:

  • Clec12A amplifies type I IFN responses, contrary to its known inhibitory role.
  • Clec12A sensing of monosodium urate (MSU) crystals enhances cytosolic RNA-induced IFN-I production.
  • Mechanistically, Clec12A engages Src kinase to positively regulate the TBK1-IRF3 signaling module.
  • Clec12A-deficient mice show impaired IFN-I responses and altered outcomes in LCMV infection models.

Conclusions:

  • Clec12A acts as a positive regulator of type I IFN responses.
  • This study uncovers a novel connection between MSU crystal sensing by Clec12A and IFN-I immunity.
  • Extracellular damage-associated molecular pattern (DAMP) sensing by Clec12A shapes innate immune responses to viral infections.