biostudies-literatureShoda TNCATS NIH HHSNIDDK NIH HHSNIAID NIH HHSNIH439-453https://www.ebi.ac.uk/biostudies/studies/S-EPMC8792211biostudies-literatureUnknown162(2)<h4>Background & aims</h4>Eosinophilic esophagitis (EoE) can progress to fibrostenosis by unclear mechanisms. Herein, we investigated gene dysregulation in fibrostenotic EoE, its association with clinical parameters and specific pathways, and the functional consequences.<h4>Methods</h4>Esophageal biopsies from subjects with EoE were collected across 11 Consortium of Eosinophilic Gastrointestinal Disease Researchers sites (n = 311) and 2 independent replication cohorts (n = 83). Inclusion criteria for fibrostenotic EoE were endoscopic rings, stricture, and/or a history of dilation. Endoscopic, histologic, and molecular features were assessed by the EoE Endoscopic Reference Score, EoE Histology Scoring System, EoE Diagnostic Panel, and RNA sequencing. Esophageal endothelial TSPAN12 expressioGastroenterologyLoss of Endothelial TSPAN12 Promotes Fibrostenotic Eosinophilic Esophagitis via Endothelial Cell-Fibroblast Crosstalk.PMC8792211U54 AI117804P30 DK078392U2C TR002818K99 AI158660Bailey DWilkey LStrobel MAtkins DSpergel ARWheatley LAtkins FGonsalves NFuruta GTOsswald GAMartin EMartin LAceves SSKhosh-Hemmat ESpergel JMHiremath GKnowles JKyle SNhu QPeterson KArva NCFoss KFelton JMKrischer JBonis PALiacouras CFuruta GPoppendeck HCahoon JLevy MDiTommaso LBolton SHamilton FKeeley KGeno DFriedlander JDohil RFoote HChehade MGupta SKAndrews RWershil BOyibo OJYang GYSinanovic SShoda TGupta STran DKatzka DTomkinson TAceves SCollins MHHirano ISchoepfer AKodroff EEby MMingler MRivera FBesl BFleischer DAbonia JPMukkada VAWechsler JBArva NMenard-Katcher CPesek RBen-Baruch Morgenstern NTasco AThompson KTholen CWen TTylicki AMack LEMenard-Katcher PDavis CCaldwell JMCapocelli KENewbury RMendoza GKaseta TDeMarshall MSun KHolland-Thomas NMcCright-Gill TSpergel JKocher KRudman Spergel AKBerry ABurke DMack DFalk GWUrv TArrington ADellon EGreuter TPutnam PEConsortium of Eosinophilic Gastrointestinal Disease Researchers (CEGIR) Investigators GroupRothenberg MZicarelli AFulkerson PFalk GWang MLKagalwalla ABray KLeung JSheridan RKhoury PScott MAlmonte SBurger CMenard-Katcher PAMuir ASable KCapocelli KKliewer KPan ZKing EPaliana AJacinto LMinnicozzi MRothenberg MEBook WZalewski ADellon ESKlion AWechsler JMurrayPetzold CRochman MMukkada VCollins MHarris JBrown TPutnam PBonis PHarris KfalseLoss of Endothelial TSPAN12 Promotes Fibrostenotic Eosinophilic Esophagitis via Endothelial Cell-Fibroblast Crosstalk.<h4>Background & aims</h4>Eosinophilic esophagitis (EoE) can progress to fibrostenosis by unclear mechanisms. Herein, we investigated gene dysregulation in fibrostenotic EoE, its association with clinical parameters and specific pathways, and the functional consequences.<h4>Methods</h4>Esophageal biopsies from subjects with EoE were collected across 11 Consortium of Eosinophilic Gastrointestinal Disease Researchers sites (n = 311) and 2 independent replication cohorts (n = 83). Inclusion criteria for fibrostenotic EoE were endoscopic rings, stricture, and/or a history of dilation. Endoscopic, histologic, and molecular features were assessed by the EoE Endoscopic Reference Score, EoE Histology Scoring System, EoE Diagnostic Panel, and RNA sequencing. Esophageal endothelial TSPAN12 expressio2022-01-01T00:00:00Z2022 Feb2026-05-10T06:51:37.539Z2025-04-05T16:10:43.485ZS-EPMC87922113468773610.1053/j.gastro.2021.10.016