Jon D. Piganelli

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 identifies soluble LAG-3 (sLAG-3) as an early biomarker of T cell activation in type 1 diabetes, detectable before islet autoantibody development and associated with beta-cell stress and high-risk HLA genotypes.

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 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.