Decio Laks Eizirik

The paper identifies an IFN-induced PD-L1 splice variant, PD-L1Δ3, which is retained intracellularly and fails to suppress T cell activation, altering β cell immune communication in type 1 diabetes.

The paper identifies ISG15 as a key factor in viral resistance in pancreatic alpha cells, showing its protective role against coxsackievirus B1 in human islet cells.

This study shows that TYK2 inhibitors reduce islet inflammation and delay type 1 diabetes onset in mice by modulating immune and endocrine responses.

This study shows that beta cell extracellular vesicle PD-L1 increases in type 1 diabetes and inhibits CD8+ T cell activity, correlating with residual beta cell function.

This study integrates multi-omics data to identify genetic variants and molecular mechanisms associated with type 2 diabetes and highlights potential drug targets.

This study shows that m6A methylation, regulated by METTL3, controls the innate immune response in β-cells during T1D onset by modulating OAS mRNA stability.

RedRibbon is a rank-rank hypergeometric overlap method for comparing gene and transcript expression signatures, showing accuracy and efficiency on large datasets.

The paper demonstrates that TOPMed imputation improves the identification of rare variants associated with type 2 diabetes in Latino populations, leading to novel associations and better polygenic scores.

This study shows that TYK2 is critical for β-cell development by regulating KRAS and IFN responses, suggesting TYK2 inhibition as a therapeutic target for type 1 diabetes.

The paper identifies splicing QTLs in human pancreatic islets that contribute to type 2 diabetes susceptibility by affecting gene splicing and revealing novel molecular mechanisms.

The paper creates TIGER, a resource integrating RNA-seq and genotyping data from human pancreatic islets to identify eQTLs and their associations with type 2 diabetes.

The paper identifies stable reference genes for normalizing gene expression in human pancreatic beta cells under stress conditions using RNA-seq and qPCR validation.

The paper investigates lipid composition changes in insulitis models and identifies ARH3 as a regulator of beta-cell apoptosis through PLA2G6 signaling.

This study shows that pro-inflammatory cytokines reveal plasticity in β-cell regulatory landscapes and identify T1D-associated variants disrupting cytokine-responsive enhancers.