Innate immune recognition of cancer

SR Woo, L Corrales, TF Gajewski - Annual review of …, 2015 - annualreviews.org
SR Woo, L Corrales, TF Gajewski
Annual review of immunology, 2015annualreviews.org
The observation that a subset of cancer patients show evidence for spontaneous CD8+ T
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 …
The observation that a subset of cancer patients show evidence for spontaneous CD8+ T 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 γδ T cells) and also by dendritic cells and macrophages in response to damage-associated molecular patterns (DAMPs). Recent evidence has indicated that the major DAMP driving host antitumor immune responses is tumor-derived DNA, sensed by the stimulator of interferon gene (STING) pathway and driving type I IFN 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.
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