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10.1189/jlb.3A0414-210R http://scihub22266oqcxt.onion/10.1189/jlb.3A0414-210R C4226789!4226789 !25170116     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25170116 &cmd=llinks): Failed to open stream: HTTP request failed! 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Cross-talk among myeloid-derived suppressor cells, macrophages, and tumor cells impacts the inflammatory milieu of solid tumors |pdf=|usr=}}{{25170116 }} gab.com Text Cross-talk among myeloid-derived suppressor cells, macrophages, and tumor cells impacts the inflammatory milieu of solid tumors JO: J Leukoc Biol http://www.kidney.de/pget.php?&tw=1&pmid=25170116 #FOAvip MDSC and macrophages are present in most solid tumors and are important drivers of immune suppression and inflammation. It is established that cross-talk between MDSC and macrophages impacts anti-tumor immunity; however, interactions between tumor cells and MDSC or macrophages are less well studied. To examine potential interactions between these cells, we studied the impact of MDSC, macrophages, and four murine tumor cell lines on each other, both in vitro and in vivo. We focused on IL-6, IL-10, IL-12, TNF-?, and NO, as these molecules are produced by macrophages, MDSC, and many tumor cells; are present in most solid tumors; and regulate inflammation. In vitro studies demonstrated that MDSC-produced IL-10 decreased macrophage IL-6 and TNF-? and increased NO. IL-6 indirectly regulated MDSC IL-10. Tumor cells increased MDSC IL-6 and vice versa. Tumor cells also increased macrophage IL-6 and NO and decreased macrophage TNF-?. Tumor cell-driven macrophage IL-6 was reduced by MDSC, and tumor cells and MDSC enhanced macrophage NO. In vivo analysis of solid tumors identified IL-6 and IL-10 as the dominant cytokines and demonstrated that these molecules were produced predominantly by stromal cells. These results suggest that inflammation within solid tumors is regulated by the ratio of tumor cells to MDSC and macrophages and that interactions of these cells have the potential to alter significantly the inflammatory milieu within the tumor microenvironment. Twit Text FOAVip Cross-talk among myeloid-derived suppressor cells, macrophages, and tumor cells impacts the inflammatory milieu of solid tumors ????J Leukoc Biol http://www.kidney.de/pget.php?&tw=1&pmid=25170116 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25170116 #FOAvip English Wikipedia <ref>{{Cite pmid|25170116 }}</ref> Cross-talk among myeloid-derived suppressor cells, macrophages, and tumor cells impacts the inflammatory milieu of solid tumors #MMPMID25170116 Beury DW ; Parker KH ; Nyandjo M ; Sinha P ; Carter KA ; Ostrand-Rosenberg S J Leukoc Biol 2014[Dec]; 96 (6 ): 1109-18 PMID25170116 show ga MDSC and macrophages are present in most solid tumors and are important drivers of immune suppression and inflammation. It is established that cross-talk between MDSC and macrophages impacts anti-tumor immunity; however, interactions between tumor cells and MDSC or macrophages are less well studied. To examine potential interactions between these cells, we studied the impact of MDSC, macrophages, and four murine tumor cell lines on each other, both in vitro and in vivo. We focused on IL-6, IL-10, IL-12, TNF-?, and NO, as these molecules are produced by macrophages, MDSC, and many tumor cells; are present in most solid tumors; and regulate inflammation. In vitro studies demonstrated that MDSC-produced IL-10 decreased macrophage IL-6 and TNF-? and increased NO. IL-6 indirectly regulated MDSC IL-10. Tumor cells increased MDSC IL-6 and vice versa. Tumor cells also increased macrophage IL-6 and NO and decreased macrophage TNF-?. Tumor cell-driven macrophage IL-6 was reduced by MDSC, and tumor cells and MDSC enhanced macrophage NO. In vivo analysis of solid tumors identified IL-6 and IL-10 as the dominant cytokines and demonstrated that these molecules were produced predominantly by stromal cells. These results suggest that inflammation within solid tumors is regulated by the ratio of tumor cells to MDSC and macrophages and that interactions of these cells have the potential to alter significantly the inflammatory milieu within the tumor microenvironment. |Animals [MESH] |Cell Communication/*physiology [MESH] |Cell Line, Tumor [MESH] |Colonic Neoplasms/immunology/metabolism/pathology [MESH] |Disease Progression [MESH] |Gene Expression Regulation, Neoplastic/*physiology [MESH] |Inflammation [MESH] |Interleukin-10/biosynthesis/genetics/metabolism [MESH] |Interleukin-12/biosynthesis/genetics/metabolism [MESH] |Interleukin-6/biosynthesis/genetics/metabolism [MESH] |Macrophages/*physiology [MESH] |Mammary Neoplasms, Experimental/immunology/metabolism/pathology [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |Mice, Inbred C57BL [MESH] |Myeloid Cells/*physiology [MESH] |Neoplasm Transplantation [MESH] |Neoplasms, Experimental/immunology/metabolism/*pathology [MESH] |Nitric Oxide/biosynthesis/metabolism [MESH] |STAT3 Transcription Factor/physiology [MESH] |Signal Transduction/physiology [MESH] |Stromal Cells/metabolism/pathology [MESH] |Transplantation, Isogeneic [MESH] |Tumor Microenvironment/*physiology [MESH]Cross-talk among myeloid-derived suppressor cells, macrophages, and tu(epmc).pdf DeepDyve Pubget Overpricing