par Grieco, Fabio Arturo 
;Moore, Fabrice ;Vigneron, François ;Santin Gomez, Izortze ;Villate, Olatz ;Marselli, Lorella;Rondas, Dieter;Korf, Hannelie;Overbergh, Lutgart;Dotta, Francesco;Marchetti, Piero;Mathieu, Chantal;Eizirik, Decio L.
Référence Diabetologia, 57, 3, page (502-511)
Publication Publié, 2014
;Moore, Fabrice ;Vigneron, François ;Santin Gomez, Izortze ;Villate, Olatz ;Marselli, Lorella;Rondas, Dieter;Korf, Hannelie;Overbergh, Lutgart;Dotta, Francesco;Marchetti, Piero;Mathieu, Chantal;Eizirik, Decio L. Référence Diabetologia, 57, 3, page (502-511)
Publication Publié, 2014
Article révisé par les pairs
| Résumé : | Cytotoxic T cells and macrophages contribute to beta cell destruction in type 1 diabetes at least in part through the production of cytokines such as IL-1β, IFN-γ and TNF-α. We have recently shown the IL-17 pathway to be activated in circulating T cells and pancreatic islets of type 1 diabetes patients. Here, we studied whether IL-17A upregulates the production of chemokines by human pancreatic islets, thus contributing to the build-up of insulitis. |
