Engineering human Tregs to resist tacrolimus via FKBP12 gene editing

Tregs. These findings demonstrate that the antiproliferative effect of tacrolimus on Tregs is critically dependent on FKBP12, mirroring its mechanism in conventional T cells. By genetically uncoupling tacrolimus from its target in Tregs, this approach suggests a strategy to preserve Treg numbers during tacrolimus-based immunosuppression in transplant recipients, potentially enhancing Treg-based therapies for transplantation tolerance.