About: SHIP deficiency causes Crohn's disease-like ileitis

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An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	SHIP deficiency causes Crohn's disease-like ileitis
Creator	Maubert, Monique Park, Mi-Young Engelman, Robert Kerr, William
Source	Medline; PMC
abstract	BACKGROUND: Inflammatory bowel disease (IBD) can arise from genetic mutations that compromise intestinal epithelial cell integrity or immune regulation. SHIP has previously been shown to play a pivotal role in limiting the number of immunoregulatory cells and their function. AIM: To determine whether SHIP plays a pivotal role in control of immune tolerance in the gut mucosa. METHODS: Gastrointestinal pathology was assessed in three separate strains of SHIP-deficient mice and their respective wild-type (WT) littermates. Gastrointestinal pathology was analysed in SHIP-deficient hosts reconstituted with WT haematopoietic cell grafts, and WT hosts reconstituted with SHIP-deficient haematopoietic cell grafts including whole splenocytes, purified T cells or natural killer (NK) cells. Major immune cell populations were also analysed in the small intestine of SHIP-deficient mice and WT controls. RESULTS: SHIP-deficient mice developed segmental, transmural pyo-granulomatous ilietis that recapitulated classical features of Crohn's disease enteric pathology. Analysis of haematopoietic chimeras showed that WT bone marrow reconstitution of SHIP(−/−) hosts corrects ileitis. Reconstitution with SHIP(−/−) splenocytes transferred ileitis to WT hosts. Adoptive transfer of purified SHIP(−/−) T cells or NK cells to WT hosts did not transfer ileitis. There was a paucity of both CD4 and CD8 T cells in the small intestines of SHIP-deficient mice; however, neutrophil numbers were significantly increased. CONCLUSIONS: SHIP plays a pivotal role in immune function in the intestine; further scrutiny of this pathway in IBD patients is warranted. It is proposed that SHIP-deficient ileitis results from a local deficit in mucosal T cell immunity that promotes a damaging granulocyte–monocyte inflammation of the distal ileum.
has issue date	2010-10-12(xsd:dateTime)
bibo:doi	10.1136/gut.2009.202283
bibo:pmid	20940287
has license	cc-by-nc
sha1sum (hex)	3cf33ae7aecff3052d051eefe7f4d26287c0217d
schema:url	https://doi.org/10.1136/gut.2009.202283
resource representing a document's title	SHIP deficiency causes Crohn's disease-like ileitis
has PubMed Central identifier	PMC3022365
has PubMed identifier	20940287
schema:publication	Gut
resource representing a document's body	covid:3cf33ae7aecff3052d051eefe7f4d26287c0217d#body_text
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