Peripheral and islet interleukin-17 pathway activation characterizes human autoimmune diabetes and promotes cytokine-mediated beta-cell death.

Arif, Sefina; Moore, Fabrice; Marks, Katherine; Bouckenooghe, Thomas; Dayan, Colin M; Planas, Raquel; Vives-Pi, Marta; Powrie, Jake; Tree, Timothy; Marchetti, Piero; Huang, Guo Cai; Gurzov, Esteban Nicolas; Pujol-Borrell, Ricardo; Eizirik, Decio L.; Peakman, Mark

doi:doi/10.2337/db10-1643

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Peripheral and islet interleukin-17 pathway activation characterizes human autoimmune diabetes and promotes cytokine-mediated beta-cell death.

par Arif, Sefina ;Moore, Fabrice

;Marks, Katherine ;Bouckenooghe, Thomas

;Dayan, Colin M ;Planas, Raquel ;Vives-Pi, Marta ;Powrie, Jake ;Tree, Timothy ;Marchetti, Piero ;Huang, Guo Cai ;Gurzov, Esteban Nicolas

;Pujol-Borrell, Ricardo ;Eizirik, Decio L.

;Peakman, Mark
Référence Diabetes (New York, N.Y.), 60, 8, page (2112-2119)
Publication Publié, 2011

Article révisé par les pairs

Résumé :

CD4 T-cells secreting interleukin (IL)-17 are implicated in several human autoimmune diseases, but their role in type 1 diabetes has not been defined. To address the relevance of such cells, we examined IL-17 secretion in response to β-cell autoantigens, IL-17A gene expression in islets, and the potential functional consequences of IL-17 release for β-cells.

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