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Learn MoreProinflammatory cytokines are important mediators of pancreatic beta cell dysfunction and demise in type 1 diabetes (T1D). We presently characterized human beta cell responses to IFNa by combining ATAC-seq, RNA-seq and proteomics assays. The initial beta cell response to IFNa was characterized by major chromatin remodeling, followed by marked changes in transcriptional and translational regulation. IFNa-induced changes in alternative splicing (AS) and first exon usage increased the diversity of transcripts expressed by beta cells. This, combined with changes observed on protein modification/degradation, ER stress and MHC class I, may significantly expand the peptide repertoire presented by beta cells to the immune system. On the other hand, beta cells up-regulated checkpoint proteins, such as PDL1 and HLA-E, that may protect them against the autoimmune assault. Data mining of the present multi-omics analysis led to the identification of two compound classes that revert IFNa effects on human beta cells and may be translated to clinical trials. SOURCE: Maikel,Luis,Colli (mcolli@ulb.ac.be) - Center for Diabetes Research Universite Libre de Bruxelles
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