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Systemic inflammation: Cancer's long-distance reach to maximize metastasis

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Article: e1075694 | Received 17 Jul 2015, Accepted 17 Jul 2015, Published online: 26 Feb 2016

Figures & data

Figure 1. Mammary tumor-activated γδ T cells educate immunosuppressive neutrophils to advance metastasis. IL1β released into the circulation by mammary tumors activates γδ T cells to produce IL17. An unknown cell type responds to IL17 by upregulating G-CSF, causing neutrophil expansion and polarization toward an immunosuppressive phenotype. Through an iNOS-dependent mechanism, neutrophils dampen CD8+ T cell killer functions so that disseminated cancer cells are protected from attack.

Figure 1. Mammary tumor-activated γδ T cells educate immunosuppressive neutrophils to advance metastasis. IL1β released into the circulation by mammary tumors activates γδ T cells to produce IL17. An unknown cell type responds to IL17 by upregulating G-CSF, causing neutrophil expansion and polarization toward an immunosuppressive phenotype. Through an iNOS-dependent mechanism, neutrophils dampen CD8+ T cell killer functions so that disseminated cancer cells are protected from attack.

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