Autoimmune diseases with high population prevalence such as type 1 diabetes (T1D) develop as a result of ill-defined interactions between putative environmental triggers and a constellation of genetic elements scattered throughout the genome. In T1D, these interactions somehow trigger a loss of tolerance to pancreatic beta cells, manifested in the form of a chronic autoimmune response that mobilizes virtually every cell type of the immune system and progressively erodes the host's beta cell mass. The five accompanying review articles focus on key areas of T1D research, ranging from genetics and pathogenesis to prediction and therapy. Here, I attempt to integrate and bring into focus the most salient points of these reviews in the context of other findings, with an emphasis on identifying knowledge gaps and research opportunities.
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