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Inflammasome

Turning on and off NLRP3

Nature Reviews Immunology volume 13, page 1 (2013)Cite this article

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IFNγ-induced NO was shown to have a specific role in regulating the production of active IL-1β

Previous studies have implicated a role for extracellular cations in the regulation of the NLRP3 inflammasome, so Lee et al. focused on the role of Ca2+ in inflammasome activation. They found that exposure of lipopolysaccharide (LPS)-primed bone marrow-derived macrophages (BMDMs) to extracellular Ca2+ induced IL-1β secretion through the calcium-sensing receptor (CASR). This effect of Ca2+ was specific for the NLRP3 inflammasome and did not activate the AIM2 or NLRC4 inflammasomes. Of note, CASR is also required for IL-1β processing in response to other NLRP3 activators.

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ORIGINAL RESEARCH PAPERS

  1. Lee, G.-S. et al. The calcium-sensing receptor regulates the NLRP3 inflammasome through Ca2+ and cAMP. Nature 11 Nov 2012 (doi:10.1038/nature11588)

  2. Mishra, B. B. et al. Nitric oxide controls the immunopathology of tuberculosis by inhibiting NLRP3 inflammasome-dependent processing of IL-1β. Nature Immunol. 18 Nov 2012 (doi:10.1038/ni.2474)

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  1. Olive Leavy
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Leavy, O. Turning on and off NLRP3. Nat Rev Immunol 13, 1 (2013). https://doi.org/10.1038/nri3366

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