Abstract
Antibody agonists targeting tumor necrosis factor (TNF) superfamily receptors, including CD40, are being tested therapeutically as anticancer agents. Studies in mice have shown that anti-CD40 monoclonal antibody (mAb) requires Fc-receptor (FcR) engagement to activate antitumor immunity. In contrast, we have reported that clinically active anti-human CD40 mAb CP-870,893 does not require FcR crosslinking, a finding with translational implications.