Innate Immune Recognition of Cancer

The observation that a subset of cancer patients show evidence for spontaneous (CD8(+). cell priming against tumor-associated antigens has generated renewed interest in the innate immune pathways that might serve as a bridge to an adaptive immune response to tumors. Manipulation of this endogenous T cell response with therapeutic intent for example, using blocking antibodies inhibiting PD-1/PD-L1 (programmed death-1 /programmed death ligand 1) interactions is showing impressive clinical results. As such, understanding the innate immune mechanisms that enable this T cell response has important clinical relevance. Defined innate immune interactions in the cancer context include recognition by innate cell populations (NK cells, NKT cells, and.y,f) '1' cells) and also by dendritic cells and macrophages in response to damage-associated molecular patterns (DAM Ps). Recent evidence has indicated that the major DAMP driving host antitumor immune responses is tumor-derived DNA, sensed by the stimulator of interferon gene (SI'ING) pathway and driving type I IF-N production. A deeper knowledge of the clinically relevant innate immune pathways involved in the recognition of tumors is leading toward new therapeutic strategies for cancer treatment.