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10.1016/j.immuni.2016.06.009 http://scihub22266oqcxt.onion/10.1016/j.immuni.2016.06.009 C4956513!4956513!27421703     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27421703&cmd=llinks): Failed to open stream: HTTP request failed! 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Interleukin-13 activates distinct cellular pathways leading to ductular reaction, steatosis, and fibrosis |pdf=|usr=}}{{27421703}} gab.com Text Interleukin-13 activates distinct cellular pathways leading to ductular reaction, steatosis, and fibrosis JO: Immunity http://www.kidney.de/pget.php?&tw=1&pmid=27421703 #FOAvip Fibroproliferative diseases are driven by dysregulated tissue repair responses and are major cause of morbidity and mortality as they affect nearly every organ system. Type-2 cytokine responses are critically involved in tissue repair; however, the mechanisms that regulate beneficial regeneration versus pathological fibrosis are not well understood. Here, we have shown that the type-2 effector cytokine interleukin-13 simultaneously, yet independently, directed hepatic fibrosis and the compensatory proliferation of hepatocytes and biliary cells in progressive models of liver disease induced by interleukin-13 over-expression or following infection with Schistosoma mansoni. Using transgenic mice with interleukin-13 signaling genetically disrupted in hepatocytes, cholangiocytes, or resident tissue fibroblasts, we have revealed direct and distinct roles for interleukin-13 in fibrosis, steatosis, cholestasis, and ductular reaction. Together, these studies show that these mechanisms are simultaneously controlled but distinctly regulated by interleukin-13 signaling. Thus, it may be possible to promote interleukin-13-dependent hepatobiliary expansion without generating pathological fibrosis. Twit Text FOAVip Interleukin-13 activates distinct cellular pathways leading to ductular reaction, steatosis, and fibrosis ????Immunity http://www.kidney.de/pget.php?&tw=1&pmid=27421703 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27421703 #FOAvip English Wikipedia <ref>{{Cite pmid|27421703}}</ref> Interleukin-13 activates distinct cellular pathways leading to ductular reaction, steatosis, and fibrosis #MMPMID27421703 Gieseck RL; Ramalingam TR; Hart KM; Vannella KM; Cantu DA; Lu WY; Ferreira-González S; Forbes SJ; Vallier L; Wynn TA Immunity 2016[Jul]; 45 (1): 145-58 PMID27421703show ga Fibroproliferative diseases are driven by dysregulated tissue repair responses and are major cause of morbidity and mortality as they affect nearly every organ system. Type-2 cytokine responses are critically involved in tissue repair; however, the mechanisms that regulate beneficial regeneration versus pathological fibrosis are not well understood. Here, we have shown that the type-2 effector cytokine interleukin-13 simultaneously, yet independently, directed hepatic fibrosis and the compensatory proliferation of hepatocytes and biliary cells in progressive models of liver disease induced by interleukin-13 over-expression or following infection with Schistosoma mansoni. Using transgenic mice with interleukin-13 signaling genetically disrupted in hepatocytes, cholangiocytes, or resident tissue fibroblasts, we have revealed direct and distinct roles for interleukin-13 in fibrosis, steatosis, cholestasis, and ductular reaction. Together, these studies show that these mechanisms are simultaneously controlled but distinctly regulated by interleukin-13 signaling. Thus, it may be possible to promote interleukin-13-dependent hepatobiliary expansion without generating pathological fibrosis. äInterleukin-13 activates distinct cellular pathways leading to ductula(epmc).pdf DeepDyve Pubget Overpricing