LAUSR

Novel immunotherapeutic concepts, including immune checkpoint inhibitors of PD-1 and CTLA-4, have dramatically changed clinical practice in cancer treatment. These therapies (re)invigorate T-cell-based tumor immune responses. However, for many patients these therapies fail, as the immunosuppressive tumor milieu often compromises initial development of spontaneous immune responses. To initiate adaptive immune responses, APCs—particularly dendritic cells (DCs)—have to engulf, process, and present tumor-associated antigens to T cells. This cross-priming of tumor-reactive T cells is dependent on DC maturation by type I interferon (IFN-I) signaling [1]. In contrast to infections, lack of proinflammatory signals in the tumor microenvironment often results in suboptimal DC activation. However, under certain circumstances, tumor cells can