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
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...
August 2015: Nature Immunology