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10.1016/j.celrep.2015.08.033

http://scihub22266oqcxt.onion/10.1016/j.celrep.2015.08.033
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C4581986!4581986!26365184
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suck abstract from ncbi


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pmid26365184      Cell+Rep 2015 ; 12 (11): 1902-14
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  • TNF counterbalances the emergence of M2 tumor macrophages #MMPMID26365184
  • Kratochvill F; Neale G; Haverkamp JM; de Velde LAV; Smith AM; Kawauchi D; McEvoy J; Roussel MF; Dyer MA; Qualls JE; Murray PJ
  • Cell Rep 2015[Sep]; 12 (11): 1902-14 PMID26365184show ga
  • Cancer is a form of 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.
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