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Autoimmune diabetes in the popular nonobese diabetic (NOD) mouse results from a T-cell–mediated destruction of the insulin-producing β-cells (1) and serves as a model for human type 1 diabetes (2,3). The mechanisms that initiate early peri-islet inflammation and the destructive components that arise later specifically targeting β-cells occur naturally in NOD mice (2,3). Two obstacles hinder our progress in unraveling the rudiments of type 1 diabetes: 1 ) the identification of the antigens involved in the earliest stages of autoimmunity and 2 ) the event(s) that provokes the initial autoimmunity and loss of homeostasis in the islets. The hope has been that the former would aid in sorting out the latter.The NOD mouse provides us with a framework for understanding T-cell–mediated autoimmune diseases in general. Discovering the nature of the initial organ-infiltrating cells is a key to the prevention of inflammatory autoimmune disease. Does spontaneous insulitis, which precedes type 1 diabetes, begin by a random accumulation of lymphocytes into the pancreatic islets, or is there an essential temporal pattern to the activation and recruitment of organ-specific lymphocytes? An answer to this question seems essential to our grasping the complexities of disease susceptibility and onset. Infectious agents have long been postulated to have a role as incendiary triggers for abnormal tissue inflammation and the genesis of a tissue-specific adaptive autoimmune/immune response. Either through …

Are T-Cell Responses to GAD65 Influential in Type 1 Diabetes?