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DEXI, a candidate gene for type 1 diabetes, modulates rat and human pancreatic beta cell inflammation via regulation of the type I IFN/STAT signalling pathway.

par Dos Santos, Reinaldo Sousa;Marroqui, Laura;Velayos, Teresa;Olazagoitia-Garmendia, Ane;Jauregi-Miguel, Amaia;Castellanos-Rubio, Ainara;Eizirik, Decio L. ;Castaňo, Luis;Santin, Izortze
Référence Diabetologia
Publication Publié, 2018-11

Article révisé par les pairs

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Résumé :

The initial stages of type 1 diabetes are characterised by an aberrant islet inflammation that is in part regulated by the interaction between type 1 diabetes susceptibility genes and environmental factors. Chromosome 16p13 is associated with type 1 diabetes and CLEC16A is thought to be the aetiological gene in the region. Recent gene expression analysis has, however, indicated that SNPs in CLEC16A modulate the expression of a neighbouring gene with unknown function named DEXI, encoding dexamethasone-induced protein (DEXI). We therefore evaluated the role of DEXI in beta cell responses to 'danger signals' and determined the mechanisms involved.