Engineering Human Tregs to Resist Tacrolimus via FKBP12 Gene Editing
Our objective is to engineer human Tregs that can resist tacrolimus without losing their identity. The central hypothesis is that tacrolimus antiproliferative effect is FKBP12 dependent by deleting FKBP12, we decouple calcineurin NFAT inhibition from Treg proliferation while preserving lineage identity.