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Significance Type 1 diabetes (T1D) is an increasing medical health problem caused by autoimmune T cells killing insulin-producing β cells in the islets of Langerhans. When the majority of β cells are destroyed, unless exogenous insulin is administered, ketoacidosis and death follow. However, providing exogenous insulin does not prevent the resultant complications of stroke, heart disease, visual impairment, or faulty wound healing, indicating the need to preserve β cells in the prediabetic stage to insure endogenous insulin production. We show that blockage of IFN-α signaling prior to clinical T1D disease by antibody or a sphingosine-1 receptor agonist prevents autoaggressive T cells from entering the islets and killing β cells. The result is aborting T1D by acting at the prediabetic stage.

Progression of type 1 diabetes from the prediabetic stage is controlled by interferon-α signaling