Optimized CRISPR-Mediated Gene Knockin Reveals FOXP3-Independent Maintenance of Human Treg Identity

To establish a benchmark of human Treg dysfunction, researchers targeted the master transcription factor FOXP3 in naive and memory Tregs. Although FOXP3-ablated Tregs upregulated cytokine expression, effects on suppressive capacity in vitro manifested slowly and primarily in memory Tregs.