Format

Send to

Choose Destination
See comment in PubMed Commons below
Nat Immunol. 2015 Aug;16(8):859-70. doi: 10.1038/ni.3202. Epub 2015 Jun 22.

The receptor NLRP3 is a transcriptional regulator of TH2 differentiation.

Author information

  • 11] Inserm, U866, Dijon, France. [2] Faculté de Médecine, Université de Bourgogne, Dijon, France.
  • 21] Inserm, U866, Dijon, France. [2] Faculté de Médecine, Université de Bourgogne, Dijon, France. [3] Centre Georges François Leclerc, Dijon, France.
  • 3Artimmune, Orleans, France.
  • 4Laboratory of Experimental and Molecular Immunology and Neurogenetics, UMR 7355 CNRS-University of Orleans, Orleans, France.

Abstract

The receptor NLRP3 is involved in the formation of the NLRP3 inflammasome that activates caspase-1 and mediates the release of interleukin 1β (IL-1β) and IL-18. Whether NLRP3 can shape immunological function independently of inflammasomes is unclear. We found that NLRP3 expression in CD4(+) T cells specifically supported a T helper type 2 (TH2) transcriptional program in a cell-intrinsic manner. NLRP3, but not the inflammasome adaptor ASC or caspase-1, positively regulated a TH2 program. In TH2 cells, NLRP3 bound the Il4 promoter and transactivated it in conjunction with the transcription factor IRF4. Nlrp3-deficient TH2 cells supported melanoma tumor growth in an IL-4-dependent manner and also promoted asthma-like symptoms. Our results demonstrate the ability of NLRP3 to act as a key transcription factor in TH2 differentiation.

PMID:
26098997
DOI:
10.1038/ni.3202
[PubMed - indexed for MEDLINE]

Publication Types, MeSH Terms, Substances, Secondary Source ID

PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Nature Publishing Group
    Loading ...
    Support Center