T cell TET2 disruption cuts the breaks on antitumor CAR T cell therapy

摘要

Functional persistence of chimeric antigen receptor (CAR) T cells is re-quired for sustaining an antitumor response. Recently, Jain et al. re-vealed that disruption of TET2 in CAR T cells resulted in antigen -independent CAR T cell hyper-proliferation that enhanced tumor control in mice, highlighting the potential of epigenetic strategies to improve T cell-based cancer immunotherapy.