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10.1053/j.gastro.2015.02.002 http://scihub22266oqcxt.onion/10.1053/j.gastro.2015.02.002 C4409569!4409569!25666870     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Gastroenterology 2015 ; 148 (6): 1143-57 Nephropedia Template TP {{tp|p=25666870|t=2015. Molecular, Genetic, and Cellular Bases for Treating Eosinophilic Esophagitis |pdf=|usr=}}{{25666870}} gab.com Text Molecular, Genetic, and Cellular Bases for Treating Eosinophilic Esophagitis JO: Gastroenterology http://www.kidney.de/pget.php?&tw=1&pmid=25666870 #FOAvip Eosinophilic esophagitis (EoE) was historically distinguished from gastroesophageal reflux disease on the basis of histology and lack of responsiveness to acid suppressive therapy, but it is now appreciated that esophageal eosinophilia can respond to proton pump inhibitors. Genetic and environmental factors contribute to risk for EoE?particularly early-life events. Disease pathogenesis involves activation of epithelial inflammatory pathways (production of eotaxin-3 [encoded by CCL26]), impaired barrier function (mediated by loss of desmoglein-1), increased production and/or activity of transforming growth factor-?, and induction of allergic inflammation by eosinophils and mast cells. Susceptibility has been associated with variants at 5q22 (TSLP) and 2p23 (CAPN14), indicating roles for allergic sensitization and esophageal specific protease pathways. We propose that EoE is a unique disease characterized by food hypersensitivity, strong hereditability influenced by early-life exposures and esophageal specific genetic risk variants, and allergic inflammation and that the disease is remitted by disrupting inflammatory and T-helper type 2 cytokine?mediated responses and through dietary elimination therapy. Twit Text FOAVip Molecular, Genetic, and Cellular Bases for Treating Eosinophilic Esophagitis ????Gastroenterology http://www.kidney.de/pget.php?&tw=1&pmid=25666870 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25666870 #FOAvip English Wikipedia <ref>{{Cite pmid|25666870}}</ref> Molecular, Genetic, and Cellular Bases for Treating Eosinophilic Esophagitis #MMPMID25666870 Rothenberg ME Gastroenterology 2015[May]; 148 (6): 1143-57 PMID25666870show ga Eosinophilic esophagitis (EoE) was historically distinguished from gastroesophageal reflux disease on the basis of histology and lack of responsiveness to acid suppressive therapy, but it is now appreciated that esophageal eosinophilia can respond to proton pump inhibitors. Genetic and environmental factors contribute to risk for EoE?particularly early-life events. Disease pathogenesis involves activation of epithelial inflammatory pathways (production of eotaxin-3 [encoded by CCL26]), impaired barrier function (mediated by loss of desmoglein-1), increased production and/or activity of transforming growth factor-?, and induction of allergic inflammation by eosinophils and mast cells. Susceptibility has been associated with variants at 5q22 (TSLP) and 2p23 (CAPN14), indicating roles for allergic sensitization and esophageal specific protease pathways. We propose that EoE is a unique disease characterized by food hypersensitivity, strong hereditability influenced by early-life exposures and esophageal specific genetic risk variants, and allergic inflammation and that the disease is remitted by disrupting inflammatory and T-helper type 2 cytokine?mediated responses and through dietary elimination therapy. äMolecular, Genetic, and Cellular Bases for Treating Eosinophilic Esoph(epmc).pdf DeepDyve Pubget Overpricing