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Related Experiment Video

Updated: Feb 2, 2026

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
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RORγ regulates the NLRP3 inflammasome.

Cyrielle Billon1, Meghan H Murray2, Amer Avdagic1

  • 1Center for Clinical Pharmacology, Washington University School of Medicine and St. Louis College of Pharmacy, St. Louis, Missouri 63110.

The Journal of Biological Chemistry
|November 21, 2018
PubMed
Summary

RAR-related orphan receptor γ (RORγ) regulates innate immunity by modulating the NLRP3 inflammasome. Inhibiting RORγ with inverse agonists reduces IL-1β secretion and may treat inflammatory diseases.

Keywords:
drug discoveryinflammasomeinnate immunityinterleukin 1 (IL-1)liverliver injurymacrophagenuclear receptortranscription factor

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Area of Science:

  • Immunology
  • Molecular Biology
  • Pharmacology

Background:

  • RAR-related orphan receptor γ (RORγ) is crucial for T helper 17 (Th17) cell development.
  • The NLRP3 inflammasome processes IL-1β and drives inflammatory diseases.
  • RORγ's role in innate immunity and NLRP3 inflammasome regulation is not fully understood.

Purpose of the Study:

  • To investigate the role of RORγ in NLRP3 inflammasome activation.
  • To evaluate RORγ inverse agonists as potential therapeutics for NLRP3-associated inflammatory diseases.

Main Methods:

  • Utilized RORγ-null mice and bone marrow-derived macrophages (BMDMs).
  • Assessed IL-1β secretion and gene expression (Nlrp3, Il1b) via quantitative PCR.
  • Examined RORγ binding to Nlrp3 and Il1b promoters using chromatin immunoprecipitation.
  • Tested RORγ inverse agonists in LPS/ATP-stimulated BMDMs and mouse models of sepsis and fulminant hepatitis.

Main Results:

  • RORγ-null BMDMs showed reduced IL-1β secretion and Nlrp3/Il1b expression.
  • RORγ directly binds to ROR response elements in Nlrp3 and Il1b gene promoters.
  • RORγ inverse agonists suppressed IL-1β secretion and gene expression in BMDMs.
  • RORγ inverse agonists reduced mortality in LPS-induced sepsis and fulminant hepatitis mouse models.

Conclusions:

  • RORγ plays a significant role in regulating NLRP3 inflammasome activity and innate immune responses.
  • Targeting RORγ with inverse agonists represents a promising therapeutic strategy for NLRP3-associated inflammatory conditions.