Abstract
Type 1 diabetes (T1D) is a metabolic disease caused by the autoimmune-mediated destruction of pancreatic β-cells; however, recent findings indicate that intrinsic stress pathways within β-cells may contribute to the initiation or perpetuation of autoimmunity. Here, we discuss the molecular and inflammatory etiologies of β-cell dysfunction in T1D, with a focus on cytokine signaling, endoplasmic reticulum stress, mitochondrial dysfunction, and senescence.