TNFRSF1B and neoplasm: Similarly, while intra-tumoral depletion of Treg cells was recently found to contribute to the anti-tumor activity of CTLA-4 mAbs in mouse models [42], intra-tumoral and splenic Treg populations were not significantly depleted by TNFR2 mAbs, and the hamster anti-TNFR2 mAbs used here did not bind detectably to mouse FcγRI or FcγRIV, indicating these mAbs are unlikely to induce ADCP (Supplementary Table S1).