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Autoimmune, or type 1 diabetes (T1D), is increasing worldwide in parallel with increases in the global standard of living. Geographically, the prevalence and incidence are diverse, explained in part by the heterogeneous distribution of HLA genetic factors on chromosome 6 that control the body’s way of dealing with infectious diseases. This may explain why some countries have a higher prevalence of T1D than others. Indeed, while Japan has relatively low levels of T1D, other countries such as Finland and Sweden are more heavily affected. The disease may affect a person at any age and the severity of the clinical onset loss of β-cells is highly variable (Fig. 1). As there are no screening programs for HLA risk and islet autoantibodies that predict the disease, the vast majority of T1D patients are not recognized until the day of clinical diagnosis (1,2).FIG. 1. Relationship between insulin release in relation to the remaining β-cell mass. Research subjects entering an intervention trial at 8–35 years of age at the time of clinical diagnosis, such as the Protege trial, may have vastly different baselines that may affect treatment and outcome. Subjects to the left may have lost a major proportion of their β-cells but still remain asymptomatic due to well-functioning β-cells and high insulin sensitivity. Subjects to the right may develop diabetes due to poor β-cell function and high insulin resistance. Heterogeneity already at baseline complicates immunomodulation intervention trials in T1D. The figure is courtesy of Daniel Cook and Ian Sweet, University of Washington, Seattle, Washington.At diagnosis, patients’ β-cell function profile can vary depending on the loss of β-cells. Some younger patients may have lost essentially all β-cells and their function, while older patients may still have considerable endogenous insulin left, with their diabetes masquerading as type 2 (1). It has taken …

Depleting T Cells in Newly Diagnosed Autoimmune (Type 1) Diabetes—Are We Getting Anywhere?