{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T05:57:17Z","timestamp":1790661437740,"version":"4.1.0"},"reference-count":121,"publisher":"MDPI AG","issue":"9","license":[{"start":{"date-parts":[[2017,9,16]],"date-time":"2017-09-16T00:00:00Z","timestamp":1505520000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Crohn\u2019s disease (CD) and ulcerative colitis (UC) are immunologically-mediated, debilitating conditions resulting from destructive inflammation of the gastrointestinal tract. The pathogenesis of IBD is incompletely understood, but is considered to be the result of an abnormal immune response with a wide range of cell types and proteins involved. Natural Killer Group 2D (NKG2D) is an activating receptor constitutively expressed on human Natural Killer (NK), \u03b3\u03b4 T, mucosal-associated invariant T (MAIT), CD56+ T, and CD8+ T cells. Activation of NKG2D triggers cellular proliferation, cytokine production, and target cell killing. Research into the NKG2D mechanism of action has primarily been focused on cancer and viral infections where cytotoxicity evasion is a concern. In human inflammatory bowel disease (IBD) this system is less characterized, but the ligands have been shown to be highly expressed during intestinal inflammation and the following receptor activation may contribute to tissue degeneration. A recent phase II clinical trial showed that an antibody against NKG2D induced clinical remission of CD in some patients, suggesting NKG2D and its ligands to be of importance in the pathogenesis of CD. This review will describe the receptor and its ligands in intestinal tissues and the clinical potential of blocking NKG2D in Crohn\u2019s disease.<\/jats:p>","DOI":"10.3390\/ijms18091997","type":"journal-article","created":{"date-parts":[[2017,9,19]],"date-time":"2017-09-19T07:12:50Z","timestamp":1505805170000},"page":"1997","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":32,"title":["Anti-NKG2D mAb: A New Treatment for Crohn\u2019s Disease?"],"prefix":"10.3390","volume":"18","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4041-0536","authenticated-orcid":false,"given":"Kasper","family":"Vadstrup","sequence":"first","affiliation":[{"name":"Gastro unit, Medical Division, Hvidovre University Hospital, Ketteg\u00e5rd Alle 30, DK-2650 Hvidovre, Denmark"},{"name":"Medical Affairs, Janssen Immunology, Janssen-Cilag A\/S, Bregner\u00f8dvej 133, DK-3460 Birker\u00f8d, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Flemming","family":"Bendtsen","sequence":"additional","affiliation":[{"name":"Gastro unit, Medical Division, Hvidovre University Hospital, Ketteg\u00e5rd Alle 30, DK-2650 Hvidovre, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2017,9,16]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"1741","DOI":"10.1016\/S0140-6736(16)31711-1","article-title":"Crohn\u2019s disease","volume":"389","author":"Torres","year":"2017","journal-title":"Lancet"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"467","DOI":"10.1016\/j.autrev.2014.01.029","article-title":"Diagnosis and classification of Crohn\u2019s disease","volume":"13","author":"Laass","year":"2014","journal-title":"Autoimmun. 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