Emily Kristen Sims

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

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 paper demonstrates that expressing human sialyltransferase in pigs reduces immune rejection by altering sialic acid linkages, improving xenotransplantation outcomes.

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.