IFN-α induces a preferential long-lasting expression of MHC class I in human pancreatic beta cells.

ABSTRACT:

Aims/hypothesis

IFN-α, a cytokine expressed in human islets from individuals affected by type 1 diabetes, plays a key role in the pathogenesis of diabetes by upregulating inflammation, endoplasmic reticulum (ER) stress and MHC class I overexpression, three hallmarks of islet histology in early type 1 diabetes. We tested whether expression of these mediators of beta cell loss is reversible upon IFN-α withdrawal or IFN-α pathway inhibition.

Methods

IFN-α-induced MHC class I overexpression, ER stress and inflammation were evaluated by flow cytometry, immunofluorescence and real-time PCR in human EndoC-βH1 cells or human islets exposed to IFN-α with or without the presence of Janus kinase (JAK) inhibitors. Protein expression was evaluated by western blot.

Results

IFN-α-in

SUBMITTER: Coomans de Brachene A 

PROVIDER: S-EPMC6241216 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature