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Few spontaneous animal models of esophageal eosinophilia exist, with most studies relying on artificial sensitization procedures. NF-\u03baB-inducing kinase (NIK; MAP3K14) is a key signaling molecule of the noncanonical NF-\u03baB (NFKB1) pathway, an alternative signaling cascade producing chemokines involved in lymphoid stroma development and leukocyte trafficking. Nik\u2212\/\u2212 mice have been shown to develop a hypereosinophilic syndrome in peripheral blood and major filtering organs; however, the gastrointestinal mucosa of these mice has not been well characterized. We show that Nik\u2212\/\u2212 mice develop significant, localized eosinophilic esophagitis that mimics human EoE, including features such as severe eosinophil accumulation, degranulation, mucosal thickening, fibrosis and basal cell hyperplasia. The remainder of the GI tract, including the caudal stomach, small intestine and colon, in mice with active EoE are unaffected, also similar to human patients. Gene expression patterns in esophageal tissue of Nik\u2212\/\u2212 mice mimics human EoE, with thymic stromal lymphopoetin (TSLP) in particular also elevated at the protein level. In gene expression data sets from human biopsy specimens, we further show that many genes associated with noncanonical NF-\u03baB signaling are significantly dysregulated in EoE patients, most notably a paradoxical upregulation of NIK itself with concurrent upregulation of powerful protein-level destabilizers of NIK. These findings suggest that Nik\u2212\/\u2212 mice could be useful as a spontaneous model of specific features of EoE and highlight a novel role for noncanonical NF-\u03baB signaling in human patients.<\/jats:p>","DOI":"10.1242\/dmm.030767","type":"journal-article","created":{"date-parts":[[2017,12,19]],"date-time":"2017-12-19T08:50:22Z","timestamp":1513673422000},"page":"1517-1527","source":"Crossref","is-referenced-by-count":25,"title":["Noncanonical NF-\u03baB signaling and the essential kinase NIK modulate crucial features associated with eosinophilic esophagitis pathogenesis"],"prefix":"10.1242","volume":"10","author":[{"given":"Kristin","family":"Eden","sequence":"first","affiliation":[{"name":"Department of Biomedical Sciences and Pathobiology, Virginia Maryland College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24060, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel E.","family":"Rothschild","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences and Pathobiology, Virginia Maryland College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24060, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dylan K.","family":"McDaniel","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences and Pathobiology, Virginia Maryland College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24060, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bettina","family":"Heid","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences and Pathobiology, Virginia Maryland College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24060, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9573-5250","authenticated-orcid":false,"given":"Irving C.","family":"Allen","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences and Pathobiology, Virginia Maryland College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24060, USA"},{"name":"Department of Biomedical Science, Virginia Tech Carilion School of Medicine, Roanoke, VA 24016, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"237","reference":[{"key":"2021042513020921200_DMM030767C1","doi-asserted-by":"publisher","first-page":"421","DOI":"10.1146\/annurev-med-041610-134138","article-title":"Eosinophilic esophagitis: rapidly advancing insights","volume":"63","author":"Abonia","year":"2012","journal-title":"Annu. 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