par Hall, Aisling O'Hara;Beiting, Daniel DP;Tato, Cristina;John, Beena;Oldenhove, Guillaume ;Lombana, Claudia Gonzalez;Pritchard, Gretchen Harms;Silver, Jonathan JS;Bouladoux, Nicolas;Stumhofer, Jason JS;Harris, Tajie H;Grainger, John;Wojno, Elia Tait ED;Wagage, Sagie;Roos, David S;Scott, Philip;Turka, Laurence LA;Cherry, Sara;Reiner, Steven SL;Cua, Daniel;Belkaid, Yasmine;Elloso, Merle MM;Hunter, Christopher A
Référence Immunity, 37, 3, page (511-523)
Publication Publié, 2012-09
Référence Immunity, 37, 3, page (511-523)
Publication Publié, 2012-09
Article révisé par les pairs
Résumé : | Interferon-γ (IFN-γ) promotes a population of T-bet(+) CXCR3(+) regulatory T (Treg) cells that limit T helper 1 (Th1) cell-mediated pathology. Our studies demonstrate that interleukin-27 (IL-27) also promoted expression of T-bet and CXCR3 in Treg cells. During infection with Toxoplasma gondii, a similar population emerged that limited T cell responses and was dependent on IFN-γ in the periphery but on IL-27 at mucosal sites. Transfer of Treg cells ameliorated the infection-induced pathology observed in Il27(-/-) mice, and this was dependent on their ability to produce IL-10. Microarray analysis revealed that Treg cells exposed to either IFN-γ or IL-27 have distinct transcriptional profiles. Thus, IFN-γ and IL-27 have different roles in Treg cell biology and IL-27 is a key cytokine that promotes the development of Treg cells specialized to control Th1 cell-mediated immunity at local sites of inflammation. |