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Cutting Edge: NF-κB Activating Pattern Recognition and Cytokine Receptors License NLRP3 Inflammasome Activation by Regulating NLRP3 Expression

The Journal of immunology (1950), 2009-07, Vol.183 (2), p.787-791 [Peer Reviewed Journal]

ISSN: 0022-1767 ;EISSN: 1550-6606 ;DOI: 10.4049/jimmunol.0901363

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  • Title:
    Cutting Edge: NF-κB Activating Pattern Recognition and Cytokine Receptors License NLRP3 Inflammasome Activation by Regulating NLRP3 Expression
  • Author: Bauernfeind, Franz G. ; Horvath, Gabor ; Stutz, Andrea ; Alnemri, Emad S. ; MacDonald, Kelly ; Speert, David ; Fernandes-Alnemri, Teresa ; Wu, Jianghong ; Monks, Brian G. ; Fitzgerald, Katherine A. ; Hornung, Veit ; Latz, Eicke
  • Is Part Of: The Journal of immunology (1950), 2009-07, Vol.183 (2), p.787-791
  • Description: Abstract The IL-1 family cytokines are regulated on transcriptional and posttranscriptional levels. Pattern recognition and cytokine receptors control pro-IL-1β transcription whereas inflammasomes regulate the proteolytic processing of pro-IL-1β. The NLRP3 inflammasome, however, assembles in response to extracellular ATP, pore-forming toxins, or crystals only in the presence of proinflammatory stimuli. How the activation of gene transcription by signaling receptors enables NLRP3 activation remains elusive and controversial. In this study, we show that cell priming through multiple signaling receptors induces NLRP3 expression, which we identified to be a critical checkpoint for NLRP3 activation. Signals provided by NF-κB activators are necessary but not sufficient for NLRP3 activation, and a second stimulus such as ATP or crystal-induced damage is required for NLRP3 activation.
  • Language: English
  • Identifier: ISSN: 0022-1767
    EISSN: 1550-6606
    DOI: 10.4049/jimmunol.0901363
  • Source: Geneva Foundation Free Medical Journals at publisher websites
    Alma/SFX Local Collection
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