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10.1016/j.celrep.2015.08.033 http://scihub22266oqcxt.onion/10.1016/j.celrep.2015.08.033 C4581986!4581986 !26365184     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26365184 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26365184 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Cell+Rep 2015 ; 12 (11 ): 1902-14 Nephropedia Template TP {{tp|p=26365184 |t=2015. TNF Counterbalances the Emergence of M2 Tumor Macrophages |pdf=|usr=}}{{26365184 }} gab.com Text TNF Counterbalances the Emergence of M2 Tumor Macrophages JO: Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=26365184 #FOAvip Cancer can involve non-resolving, persistent inflammation where varying numbers of tumor-associated macrophages (TAMs) infiltrate and adopt different activation states between anti-tumor M1 and pro-tumor M2 phenotypes. Here, we resolve a cascade causing differential macrophage phenotypes in the tumor microenvironment. Reduction in TNF mRNA production or loss of type I TNF receptor signaling resulted in a striking pattern of enhanced M2 mRNA expression. M2 gene expression was driven in part by IL-13 from eosinophils co-recruited with inflammatory monocytes, a pathway that was suppressed by TNF. Our data define regulatory nodes within the tumor microenvironment that balance M1 and M2 populations. Our results show macrophage polarization in cancer is dynamic and dependent on the balance between TNF and IL-13, thus providing a strategy for manipulating TAMs. Twit Text FOAVip TNF Counterbalances the Emergence of M2 Tumor Macrophages ????Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=26365184 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26365184 #FOAvip English Wikipedia <ref>{{Cite pmid|26365184 }}</ref> TNF Counterbalances the Emergence of M2 Tumor Macrophages #MMPMID26365184 Kratochvill F ; Neale G ; Haverkamp JM ; Van de Velde LA ; Smith AM ; Kawauchi D ; McEvoy J ; Roussel MF ; Dyer MA ; Qualls JE ; Murray PJ Cell Rep 2015[Sep]; 12 (11 ): 1902-14 PMID26365184 show ga Cancer can involve non-resolving, persistent inflammation where varying numbers of tumor-associated macrophages (TAMs) infiltrate and adopt different activation states between anti-tumor M1 and pro-tumor M2 phenotypes. Here, we resolve a cascade causing differential macrophage phenotypes in the tumor microenvironment. Reduction in TNF mRNA production or loss of type I TNF receptor signaling resulted in a striking pattern of enhanced M2 mRNA expression. M2 gene expression was driven in part by IL-13 from eosinophils co-recruited with inflammatory monocytes, a pathway that was suppressed by TNF. Our data define regulatory nodes within the tumor microenvironment that balance M1 and M2 populations. Our results show macrophage polarization in cancer is dynamic and dependent on the balance between TNF and IL-13, thus providing a strategy for manipulating TAMs. |Animals [MESH] |Cell Line, Tumor [MESH] |Gene Expression [MESH] |Macrophages/*metabolism [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Mice, Nude [MESH] |Neoplasms/*metabolism/pathology [MESH] |Signal Transduction [MESH] |Tumor Microenvironment [MESH]TNF Counterbalances the Emergence of M2 Tumor Macrophages (epmc).pdf DeepDyve Pubget Overpricing