Carmella Evans‐Molina

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 paper introduces a method using SPAD arrays to count fluorophores in widefield microscopy by modeling PCH statistics and performing Bayesian inference.

In 299 islet preparations from donors without diabetes, endocrine cell composition, not donor demographics, tracked insulin secretion, and δ cell percentage rose with type 2 diabetes genetic risk.

This study investigates how altered B cell metabolic pathways, particularly HIF-1 signaling, contribute to Type 1 Diabetes progression by shifting B cell differentiation toward inflammatory subsets.

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 paper develops a sensitive LC-MS method to quantify circulating proinsulin proteoforms and C-peptide, showing improved separation of control and T1D groups compared to ELISA.

This study shows that GPER signaling maintains β cell identity in female mice, and its loss during menopause may contribute to β cell dysfunction and T2D risk.

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 investigates how GPR17 inhibits GLP-1 secretion in enteroendocrine cells through Gi/o-dependent signaling, using pharmacological and genetic approaches.

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 miR-146a-5p overexpression in beta cells under inflammatory stress causes mitochondrial dysfunction and apoptosis, while its inhibition reverses these effects.

This study shows that HDI sodium butyrate improves β cell function and calcium signaling in diabetes by restoring STIM1 and SOCE, and inhibiting GSK-3 through AKT.

This study examines how diabetes affects the daily rhythmic gene expression in retinas, finding phase shifts in the transcriptional cycle linked to metabolic and hypoxia pathways.

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 cigarette smoke exposure impairs β-cell function through oxidative stress and ceramide accumulation, with effects persisting after smoking cessation.