Abstract

Dendritic cells (DCs) orchestrate a repertoire of immune responses that bring about resistance to infection and tolerance to self. Cancers can exploit DCs to evade immunity, but DCs also can generate resistance to cancer. Owing to their capacity to capture, process, and present antigens to naïve T cells, thereby launching adaptive immunity, DCs are poised to play a critical role in cancer recognition and rejection. As such, DCs represent a solution for the expansion and infiltration of T cells with tumor-rejecting properties. Indeed, clinical responses to checkpoint blockade, such as anti-PD-1, are linked to the presence of T cell immunity to cancer-specific antigens. However, only a fraction of patients has clinical benefit. Unraveling the molecular pathways controlling DC-cancer interplay will therefore pave the way for identifying new targets for therapy that overcome limitations of current treatments and promote long-term cancer control.

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