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Bruchard, Mélanie; Rebé, Cédric; Derangère, Valentin; Togbé, Dieudonnée; Ryffel, Bernhard; Boidot, Romain; Humblin, Etienne; Hamman, Arlette; Chalmin, Fanny; Berger, Hélène; Chevriaux, Angélique; Limagne, Emeric; Apetoh, Lionel; Végran, Frédérique; Ghiringhelli, François
Nature immunology 16, Številka: 8Journal Article
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.
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