Abstract
T1D develops after immune mediated destruction of insulin-producing β-cells. Hereby the dysregulation of adaptive immunity, in particular T-helper (Th) and regulatory cells (Tregs), plays the major role. VD insufficiency is an established risk factor and VD-supplementation in infantry is associated with reduced T1D incidence. VD-therapy in new onset, as well as chronic T1D may have beneficial immune and metabolic effects.
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