{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T11:21:40Z","timestamp":1790162500822,"version":"4.1.0"},"reference-count":74,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2020,1,27]],"date-time":"2020-01-27T00:00:00Z","timestamp":1580083200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"name":"Celiac Disease Center at Columbia University"},{"name":"Bouncer Foundation"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2020,4,16]]},"abstract":"<jats:title>Summary<\/jats:title>\n               <jats:p>The small intestinal (SI) epithelium harbors a heterogeneous population of lymphocytes that mediate mucosal damage and repair in celiac disease (CD). The composition and roles of human proximal SI intra-epithelial innate lymphoid cells (ILCs), and their alterations in CD, are not well understood. We report that duodenal intra-epithelial ILCs predominantly consist of natural killer (NK)p44+CD127\u2212 cytotoxic ILC1s and NKp44\u2212CD127+ helper ILC1s, while ILC3s only represent a minor population. In patients with newly diagnosed or active CD (ACD) and refractory CD type 1 (RCD I), the frequency of SI NKp44+ ILCs is decreased, with restoration of NKp44+ ILC frequency observed in patients adhering to a gluten-free diet who show evidence of mucosal healing. Moreover, the frequency of SI NKp44\u2212 ILCs is increased in ACD and RCD I patients and correlates with the severity of villous atrophy and epithelial damage, as assessed by serum levels of fatty acid binding protein 2 (FABP2). We show that the ILC alterations in CD represent a phenotypic shift of cytotoxic ILC1s rather than an increase in helper ILC1s or transdifferentiation of ILC1s\u00a0to ILC3s, and activation-induced loss of NKp44 by cytotoxic ILC1s is associated with increased interferon (IFN)-\u03b3 expression and release of lytic granules. These findings suggest that intra-epithelial NKp44\u2212CD127\u2212 cytotoxic ILC1s may contribute to mucosal damage in CD.<\/jats:p>","DOI":"10.1111\/cei.13414","type":"journal-article","created":{"date-parts":[[2020,1,7]],"date-time":"2020-01-07T07:41:37Z","timestamp":1578382897000},"page":"163-175","source":"Crossref","is-referenced-by-count":19,"title":["Phenotypic shift of small intestinal intra-epithelial type 1 innate lymphoid cells in celiac disease is associated with enhanced cytotoxic potential"],"prefix":"10.1093","volume":"200","author":[{"given":"M","family":"Uhde","sequence":"first","affiliation":[{"name":"Department of Medicine, Celiac Disease Center, Columbia University Irving Medical Center , New York, NY, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5659-1418","authenticated-orcid":false,"given":"X","family":"Yu","sequence":"additional","affiliation":[{"name":"Department of Medicine, Celiac Disease Center, Columbia University Irving Medical Center , New York, NY, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A","family":"Bunin","sequence":"additional","affiliation":[{"name":"Department of Medicine, Celiac Disease Center, Columbia University Irving Medical Center , New York, NY, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C","family":"Brauner","sequence":"additional","affiliation":[{"name":"Department of Medicine, Celiac Disease Center, Columbia University Irving Medical Center , New York, NY, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S K","family":"Lewis","sequence":"additional","affiliation":[{"name":"Department of Medicine, Celiac Disease Center, Columbia University Irving Medical Center , New York, NY, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B","family":"Lebwohl","sequence":"additional","affiliation":[{"name":"Department of Medicine, Celiac Disease Center, Columbia University Irving Medical Center , New York, NY, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S","family":"Krishnareddy","sequence":"additional","affiliation":[{"name":"Department of Medicine, Celiac Disease Center, Columbia University Irving Medical Center , New York, NY, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A","family":"Alaedini","sequence":"additional","affiliation":[{"name":"Department of Medicine, Celiac Disease Center, Columbia University Irving Medical Center , New York, NY, USA"},{"name":"Institute of Human Nutrition, Columbia University Irving Medical Center , New York, NY, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B","family":"Reizis","sequence":"additional","affiliation":[{"name":"Department of Pathology, Department of Medicine, New York University Langone Medical Center , New York, NY, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S","family":"Ghosh","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, College of Physicians and Surgeons, Columbia University , New York, NY, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P H","family":"Green","sequence":"additional","affiliation":[{"name":"Department of Medicine, Celiac Disease Center, Columbia University Irving Medical Center , New York, NY, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G","family":"Bhagat","sequence":"additional","affiliation":[{"name":"Department of Medicine, Celiac Disease Center, Columbia University Irving Medical Center , New York, NY, USA"},{"name":"Department of Pathology and Cell Biology, Columbia University Irving Medical Center , New York, NY, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2020,1,27]]},"reference":[{"key":"2023081612584504500_cei13414-bib-0001","doi-asserted-by":"crossref","first-page":"1731","DOI":"10.1056\/NEJMra071600","article-title":"Celiac disease","volume":"357","author":"Green","year":"2007","journal-title":"N Engl J Med"},{"key":"2023081612584504500_cei13414-bib-0002","doi-asserted-by":"crossref","first-page":"70","DOI":"10.1016\/S0140-6736(17)31796-8","article-title":"Coeliac disease","volume":"391","author":"Lebwohl","year":"2018","journal-title":"Lancet"},{"key":"2023081612584504500_cei13414-bib-0003","doi-asserted-by":"crossref","first-page":"493","DOI":"10.1146\/annurev-immunol-040210-092915","article-title":"Integration of genetic and immunological insights into a model of celiac disease pathogenesis","volume":"29","author":"Abadie","year":"2011","journal-title":"Ann Rev 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