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

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...

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Detalles Bibliográficos
Autores principales: Chiba, Shiho, Ikushima, Hiroaki, Ueki, Hiroshi, Yanai, Hideyuki, Kimura, Yoshitaka, Hangai, Sho, Nishio, Junko, Negishi, Hideo, Tamura, Tomohiko, Saijo, Shinobu, Iwakura, Yoichiro, Taniguchi, Tadatsugu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: eLife Sciences Publications, Ltd 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4161974/
https://www.ncbi.nlm.nih.gov/pubmed/25149452
http://dx.doi.org/10.7554/eLife.04177
Descripción
Sumario: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. DOI: http://dx.doi.org/10.7554/eLife.04177.001