Abstract
Abstract Using xenograft and in vitro models, anti-CD47 antibody is thought to enhance "eat me" signaling to kill tumor cells by macrophage-mediated phagocytosis. However, the potential for adaptive immune response in anti-CD47 mediated tumor control has been ignored. Here we reveal a novel mechanism in which tumor regression after local anti-CD47 antibody treatment depends on cytotoxic T lymphocyte (CTLs) response. Mechanically, tumor recognition by DC following anti-CD47 enhances type I IFNs production and that subsequent IFNs signaling strengthens the cross-priming capability of DCs within the tumor microenvironment. Intriguing, anti-CD47 mediated antitumor immunity requires adaptor protein STING for the innate sensing of tumor cells. Additionally, we delineate a clinically relevant combinational strategy of chemotherapeutic drugs and anti-CD47 antibody to enhance the reduction of tumor burden without abrogating anti-CD47 initiated immunity.
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