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10.1172/JCI64115 http://scihub22266oqcxt.onion/10.1172/JCI64115 C3484453!3484453!23064360     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Clin+Invest 2012 ; 122 (11): 4094-104 Nephropedia Template TP {{tp|p=23064360|t=2012. TNF signaling drives myeloid-derived suppressor cell accumulation |pdf=|usr=}}{{23064360}} gab.com Text TNF signaling drives myeloid-derived suppressor cell accumulation JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=23064360 #FOAvip TNF, an inflammatory cytokine that is enriched in the tumor microenvironment, promotes tumor growth and subverts innate immune responses to cancer cells. We previously reported that tumors implanted in TNF receptor?deficient (Tnfr?/?) mice are spontaneously rejected; however, the molecular mechanisms underlying this rejection are unclear. Here we report that TNF signaling drives the peripheral accumulation of myeloid-derived suppressor cells (MDSCs). MDSCs expand extensively during inflammation and tumor progression in mice and humans and can enhance tumor growth by repressing T cell?mediated antitumor responses. Peripheral accumulation of MDSCs was drastically impaired in Tnfr?/? mice. Signaling of TNFR-2, but not TNFR-1, promoted MDSC survival through upregulation of cellular FLICE-inhibitory protein (c-FLIP) and inhibition of caspase-8 activity. Loss of TNFRs impaired the induction of MDSCs from bone marrow cells, but this could be reversed by treatment with caspase inhibitors. These results demonstrate that TNFR-2 signaling promotes MDSC survival and accumulation and helps tumor cells evade the immune system. Twit Text FOAVip TNF signaling drives myeloid-derived suppressor cell accumulation ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=23064360 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23064360 #FOAvip English Wikipedia <ref>{{Cite pmid|23064360}}</ref> TNF signaling drives myeloid-derived suppressor cell accumulation #MMPMID23064360 Zhao X; Rong L; Zhao X; Li X; Liu X; Deng J; Wu H; Xu X; Erben U; Wu P; Syrbe U; Sieper J; Qin Z J Clin Invest 2012[Nov]; 122 (11): 4094-104 PMID23064360show ga TNF, an inflammatory cytokine that is enriched in the tumor microenvironment, promotes tumor growth and subverts innate immune responses to cancer cells. We previously reported that tumors implanted in TNF receptor?deficient (Tnfr?/?) mice are spontaneously rejected; however, the molecular mechanisms underlying this rejection are unclear. Here we report that TNF signaling drives the peripheral accumulation of myeloid-derived suppressor cells (MDSCs). MDSCs expand extensively during inflammation and tumor progression in mice and humans and can enhance tumor growth by repressing T cell?mediated antitumor responses. Peripheral accumulation of MDSCs was drastically impaired in Tnfr?/? mice. Signaling of TNFR-2, but not TNFR-1, promoted MDSC survival through upregulation of cellular FLICE-inhibitory protein (c-FLIP) and inhibition of caspase-8 activity. Loss of TNFRs impaired the induction of MDSCs from bone marrow cells, but this could be reversed by treatment with caspase inhibitors. These results demonstrate that TNFR-2 signaling promotes MDSC survival and accumulation and helps tumor cells evade the immune system. äTNF signaling drives myeloid-derived suppressor cell accumulation (epmc).pdf DeepDyve Pubget Overpricing