Abstract

TO THE EDITOR: Macrophage checkpoint inhibition, an approach in which the phagocytic clearance of cancer cells is reactivated, represents a new paradigm in immuno-oncology. In parallel, a defect in “efferocytosis” (i.e., the removal of inflamed and dying cells by phagocytosis) is now recognized as a hallmark of atherosclerotic disease, which is caused in part by pathologic up-regulation of the antiphagocytic signal molecule CD47. 1,2 A recent phase 1b–2 trial of a humanized anti-CD47 antibody (magrolimab) showed promising results in tumor reduction, as measured by 18 F-fluorodeoxyglucose ( 18 F-FDG) positron-emission tomography and computed tomography in patients with relapsed or refractory lymphoma. 3 Given that anti-CD47 therapies reduced atherosclerotic burden and plaque rupture in preclinical studies, 1 we hypothesized that magrolimab might reduce vascular inflammation, as quantified by 18 F-FDG uptake, in the carotid arteries of these participants.