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Elife. 2014 Aug 22;3:e04177. doi: 10.7554/eLife.04177.

Recognition of tumor cells by Dectin-1 orchestrates innate immune cells for anti-tumor responses.

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Department of Molecular Immunology, Institute of Industrial Science, The University of Tokyo, Tokyo, Japan.
Department of Immunology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Department of Molecular Immunology, Medical Mycology Research Center, Chiba University, Chiba, Japan.
Center for Animal Disease Models, Research Institute for Biomedical Sciences, Tokyo University of Science, Noda, Japan.


The eradication of tumor cells requires communication to and signaling by cells of the immune system. Natural killer (NK) cells are essential tumor-killing effector cells of the innate immune system; however, little is known about whether or how other immune cells recognize tumor cells to assist NK cells. Here, we show that the innate immune receptor Dectin-1 expressed on dendritic cells and macrophages is critical to NK-mediated killing of tumor cells that express N-glycan structures at high levels. Receptor recognition of these tumor cells causes the activation of the IRF5 transcription factor and downstream gene induction for the full-blown tumoricidal activity of NK cells. Consistent with this, we show exacerbated in vivo tumor growth in mice genetically deficient in either Dectin-1 or IRF5. The critical contribution of Dectin-1 in the recognition of and signaling by tumor cells may offer new insight into the anti-tumor immune system with therapeutic implications.


Dectin-1; IRF; NK cell; immunology; innate immunity; mouse

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