Lenvatinib-treated Tregs exhibit superior anti-inflammation effect in autoimmune diseases

Here, we identified a novel immunomodulatory function of the multi-kinase inhibitor lenvatinib (Lenv) in specifically promoting Treg differentiation without affecting other T helper cell subsets.

Mechanistically, Lenv inhibited VEGFR/AKT signaling and activated Foxo1, thereby enhancing Foxp3 expression. Adoptive transfer of Lenv-treated Tregs (Lenv-Tregs) in murine models of IBD, psoriasis, and rosacea achieved superior alleviation of clinical symptoms and inflammation compared with vehicle-treated Tregs (Ctrl-Tregs). Our findings uncover a novel role for Lenv in Treg differentiation and provide a robust strategy to generate a considerable number of highly potent immunosuppressive Tregs for cell-based therapy against AIDs.