The receptor NLRP3 is a transcriptional regulator of TH2 differentiation

Mélanie Bruchard, Cédric Rebé, Valentin Derangère, Dieudonnée Togbé, Bernhard Ryffel, Romain Boidot, Etienne Humblin, Arlette Hamman, Fanny Chalmin, Hélène Berger, Angélique Chevriaux, Emeric Limagne, Lionel Apetoh, Frédérique Végran, François Ghiringhelli

Research output: Contribution to journalArticlepeer-review

270 Scopus citations


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.

Original languageEnglish
Pages (from-to)859-870
Number of pages12
JournalNature Immunology
Issue number8
StatePublished - 21 Jul 2015
Externally publishedYes


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