Fiche publication
Date publication
août 2014
Auteurs
Membres identifiés du Cancéropôle Est :
Dr BOIDOT Romain
,
Pr GHIRINGHELLI François
,
Dr VEGRAN Frédérique
,
Dr REBE Cédric
,
Dr BRUCHARD Mélanie
,
Dr CHALMIN Fanny
,
Dr DERANGERE Valentin
Tous les auteurs :
Vegran F, Berger H, Boidot R, Mignot G, Bruchard M, Dosset M, Chalmin F, Rebe C, Derangere V, Ryffel B, Kato M, Prevost-Blondel A, Ghiringhelli F, Apetoh L
Lien Pubmed
Résumé
The TH9 subset of helper T cells was initially shown to contribute to the induction of autoimmune and allergic diseases, but subsequent evidence has suggested that these cells also exert antitumor activities. However, the molecular events that account for their effector properties are elusive. Here we found that the transcription factor IRF1 enhanced the effector function of TH9 cells and dictated their anticancer properties. Under TH9-skewing conditions, interleukin 1beta (IL-1beta) induced phosphorylation of the transcription factor STAT1 and subsequent expression of IRF1, which bound to the promoters of Il9 and Il21 and enhanced secretion of the cytokines IL-9 and IL-21 from TH9 cells. Furthermore, IL-1beta-induced TH9 cells exerted potent anticancer functions in an IRF1- and IL-21-dependent manner. Our findings thus identify IRF1 as a target for controlling the function of TH9 cells.
Référence
Nat Immunol. 2014 Aug;15(8):758-66
