Jacob R. Enriquez

This study identifies sex-specific islet responses to inflammation and shows that estrogen reduces inflammatory signaling and promotes immune tolerance in beta cells, contributing to sex differences in type 1 diabetes susceptibility.

This study identifies GPR31 as a key inflammatory regulator in pancreatic islets, showing its role in β-cell stress and macrophage activation in type 1 diabetes.

This study shows that proinflammatory stress in beta cells increases ceramide-enriched extracellular vesicles via nSMase2, which may affect paracrine signaling in diabetes.

This study shows that inhibiting the integrated stress response (ISR) reduces macrophage inflammation and migration in a mouse model of type 1 diabetes.

This study shows that inhibiting 12-LOX with VLX-1005 delays autoimmune diabetes onset in human gene replacement mice by altering inflammatory pathways and immune cell infiltration.

This study shows that inhibiting PERK reduces autoimmune diabetes risk in mice by decreasing β cell immunogenicity and improving islet function.

This study uses human organoids to show RFX6 mutations cause duodenal malformations by disrupting PDX1 and other signaling pathways.

This study uses patient-derived organoids to identify new pathologies in individuals with PDX1 mutations, revealing intestinal and gastric metaplasia.