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The receptor NLRP3 is a transcriptional regulator of TH2 differentiation.
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.
Affiliation
  • Bruchard M; 1] Inserm, U866, Dijon, France. [2] Faculté de Médecine, Université de Bourgogne, Dijon, France.
  • Rebé C; 1] Inserm, U866, Dijon, France. [2] Faculté de Médecine, Université de Bourgogne, Dijon, France. [3] Centre Georges François Leclerc, Dijon, France.
  • Derangère V; 1] Inserm, U866, Dijon, France. [2] Faculté de Médecine, Université de Bourgogne, Dijon, France. [3] Centre Georges François Leclerc, Dijon, France.
  • Togbé D; Artimmune, Orleans, France.
  • Ryffel B; Laboratory of Experimental and Molecular Immunology and Neurogenetics, UMR 7355 CNRS-University of Orleans, Orleans, France.
  • Boidot R; 1] Inserm, U866, Dijon, France. [2] Faculté de Médecine, Université de Bourgogne, Dijon, France. [3] Centre Georges François Leclerc, Dijon, France.
  • Humblin E; 1] Inserm, U866, Dijon, France. [2] Faculté de Médecine, Université de Bourgogne, Dijon, France.
  • Hamman A; 1] Inserm, U866, Dijon, France. [2] Faculté de Médecine, Université de Bourgogne, Dijon, France.
  • Chalmin F; 1] Inserm, U866, Dijon, France. [2] Faculté de Médecine, Université de Bourgogne, Dijon, France.
  • Berger H; 1] Inserm, U866, Dijon, France. [2] Faculté de Médecine, Université de Bourgogne, Dijon, France.
  • Chevriaux A; 1] Inserm, U866, Dijon, France. [2] Faculté de Médecine, Université de Bourgogne, Dijon, France. [3] Centre Georges François Leclerc, Dijon, France.
  • Limagne E; 1] Inserm, U866, Dijon, France. [2] Faculté de Médecine, Université de Bourgogne, Dijon, France.
  • Apetoh L; 1] Inserm, U866, Dijon, France. [2] Faculté de Médecine, Université de Bourgogne, Dijon, France. [3] Centre Georges François Leclerc, Dijon, France.
  • Végran F; 1] Inserm, U866, Dijon, France. [2] Faculté de Médecine, Université de Bourgogne, Dijon, France. [3] Centre Georges François Leclerc, Dijon, France.
  • Ghiringhelli F; 1] Inserm, U866, Dijon, France. [2] Faculté de Médecine, Université de Bourgogne, Dijon, France. [3] Centre Georges François Leclerc, Dijon, France.
Nat Immunol ; 16(8): 859-70, 2015 Aug.
Article in En | MEDLINE | ID: mdl-26098997
ABSTRACT
The receptor NLRP3 is involved in the formation of the NLRP3 inflammasome that activates caspase-1 and mediates the release of interleukin 1ß (IL-1ß) 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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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Carrier Proteins / Cell Differentiation / Trans-Activators / Th2 Cells Language: En Journal: Nat Immunol Journal subject: ALERGIA E IMUNOLOGIA Year: 2015 Type: Article Affiliation country: France
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Carrier Proteins / Cell Differentiation / Trans-Activators / Th2 Cells Language: En Journal: Nat Immunol Journal subject: ALERGIA E IMUNOLOGIA Year: 2015 Type: Article Affiliation country: France