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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
Wataru Amano, Saeko Nakajima, Hayato Kunugi, Yasuharu Numata, Akihiko Kitoh, Gyohei Egawa, Teruki Dainichi, Tetsuya Honda, Atsushi Otsuka, Yukari Kimoto, Yasuo Yamamoto, Atsuo Tanimoto, Mutsuyoshi Matsushita, Yoshiki Miyachi, Kenji Kabashima
BACKGROUND: Barrier disruption and the resulting continuous exposure to allergens are presumed to be responsible for the development of atopic dermatitis (AD). However, the mechanism through which skin barrier function is disrupted in patients with AD remains unclear. OBJECTIVES: Taking into account the fact that the TH2 milieu impairs keratinocyte terminal differentiation, we sought to clarify our hypothesis that the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway plays a critical role in skin barrier function and can be a therapeutic target for AD...
September 2015: Journal of Allergy and Clinical Immunology
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