Targeting the orphan nuclear receptor NR2F6 in T cells primes tumors for immune checkpoint therapy.
Victoria KlepschMaria PommermayrDominik HumerNatascha BrigoNatascha Hermann-KleiterGottfried BaierPublished in: Cell communication and signaling : CCS (2020)
These findings indicate that Nr2f6CRISPR/Cas9 knockout T cells are comparable to germline Nr2f6-/- T cells, a result providing an independent confirmation of the immune checkpoint function of lymphatic NR2F6. Taken together, CRISPR/Cas9-mediated acute Nr2f6 gene ablation in primary mouse T cells prior to ACT appeared feasible for potentiating established PD-L1 and CTLA-4 blockade therapies, thereby pioneering NR2F6 inhibition as a sensitizing target for augmented tumor regression. Video abstract.