Durable control of autoimmunity requires sustained stimulation of regulatory T cells

However, clinical benefits are limited by the suboptimal pharmacokinetic profile of rIL-2, which fails to support sustained Treg activation. Here we investigated the efficacy of a long-lasting IL-2-based biologic mIL-2/CD25 to limit type 1 diabetes in female NOD mice when administered in a manner to cause periodic versus continual increases in Tregs.

We find that the latter is highly effective in limiting autoimmunity and leads to substantial remodeling of the pancreatic islet immune landscape, which has important implications for advancing IL-2-based therapies for autoimmunity.