
The study investigates the role of B7-H3, a newer immunotherapy agent, in a preclinical melanoma model driven by β-catenin. The results show that B7-H3 confers a suppressive tumor microenvironment by modulating antiviral signals and innate immunity, and inhibition of B7-H3 leads to an inflamed microenvironment with up-regulation of CD47/SIRPa signaling. The combination of B7-H3 inhibition and blockade of the macrophage checkpoint CD47 resulted in additive antitumor responses dependent on cytokine signaling pathways (CCR5/CCL5 and IL4). The study highlights the potential of the B7-H3/CD47 antibody combination as a new effective immunotherapy strategy for T-cell non-inflamed tumors.
Like
Save
Share