par Ysebrant De Lendonck, Laure 
;Tonon, Sandrine ;Nguyen, Muriel ;Vandevenne, Patricia ;Welsby, Iain ;Martinet, Valérie ;Molle, Céline ;Charbonnier, Louis-Marie ;Leo, Oberdan ;Goriely, Stanislas
Référence Proceedings of the National Academy of Sciences of the United States of America, 110, 34, page (E3189-E3197)
Publication Publié, 2013-08
;Tonon, Sandrine ;Nguyen, Muriel ;Vandevenne, Patricia ;Welsby, Iain ;Martinet, Valérie ;Molle, Céline ;Charbonnier, Louis-Marie ;Leo, Oberdan ;Goriely, Stanislas Référence Proceedings of the National Academy of Sciences of the United States of America, 110, 34, page (E3189-E3197)
Publication Publié, 2013-08
Article révisé par les pairs
| Résumé : | IFN regulatory factor (IRF) 3 plays a key role in innate responses against viruses. Herein we assessed its contribution to T-cell activation. We observed that poly(I:C)-induced IRF3 activation in CD8 T cells represses IL-17 expression in a type I IFN-independent fashion. Even in the absence of poly(I:C), polyclonally activated naïve IRF3(-/-) CD8 T cells expressed high levels of IL-17 and IL-23R in comparison with wild-type cells. Furthermore, IRF3(-/-) OT1 cells adoptively transferred into wild-type hosts also produced higher IL-17 levels upon immunization than their wild-type counterparts. This phenotype could be reversed by ectopic expression of IRF3, confirming that this effect is intrinsic to T cells. We show that IRF3 directly interacts with RORγt in the cytoplasm through its IRF interaction domain and limits its ability to bind and transactivate the IL-17 promoter. These observations uncover an unexpected role of IRF3 in the control of CD8 T-cell polarization. |
