Raghavendra G. Mirmira

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.

This study shows dietary glutamate influences ImP production via microbial competition, affecting glucose tolerance and systemic ImP levels.

The paper identifies carbamylation as a regulatory modification in β-cell metabolism and insulin processing in T1D by analyzing proteomic changes in NOD and MIN6 cells.

This study evaluates plasma extracellular vesicle proteomics for identifying predictive biomarkers of type 1 diabetes development, finding 448 differentially abundant proteins and a 0.81 AUC in predicting islet autoimmunity.

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 investigates the distinct roles of hypusinated and unhypusinated eIF5A isoforms in pancreas development and function using zebrafish and mouse models.

This study shows that inhibiting 12-LOX improves glucose homeostasis and reduces obesity-related inflammation in human gene replacement mice.

This study shows omega-3 fatty acids reduce CXCL9 expression in MIN6 cells via ARH3, potentially protecting beta cells from immune attack and preventing T1D.

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

This study shows that deleting eIF5A or DHPS in mice causes brain development issues and cognitive impairments, with DHPS knockouts showing more severe effects.

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 loss of Robo1 and Robo2 in beta cells disrupts synchronized calcium oscillations in islets of Langerhans in vivo, indicating that islet architecture is essential for this coordination.