ArticleGut2011
SHIP deficiency causes Crohn's disease-like ileitis.
Article in Gut, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 73 citations in OpenAlex.
- SHIP1 is required for T cell surveillance of occult malignancies.Cellular and molecular life sciences : CMLS · 2026Article
- A yeast synthetic biotic platform for delivery of therapeutic nanobodies to ameliorate gastrointestinal inflammation.Disease models & mechanisms · 2026Article
- TIGIT/SHIP-1/RelB regulating Th1 inflammation in smoking induced COPD.Respiratory research · 2025Article
- Mesenteric adipose tissue in Crohn's disease alters the immune response of the ileal mucosa and increases angiogenesis and fibrosis.Scientific reports · 2025Article
- Environmental and inflammatory factors influencing concurrent gut and lung inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Genome-wide studies define new genetic mechanisms of IgA vasculitis.medRxiv : the preprint server for health sciences · 2024Article
- Regulation of Microglial Signaling by Lyn and SHIP-1 in the Steady-State Adult Mouse Brain.Cells · 2023Article
- Pathological Roles of INPP5D in Alzheimer's Disease.Advances in experimental medicine and biology · 2023Article
- Regulation of microglial responses after pediatric traumatic brain injury: exploring the role of SHIP-1.Frontiers in neuroscience · 2023Article
- Discovery of a novel SHIP1 agonist that promotes degradation of lipid-laden phagocytic cargo by microglia.iScience · 2022Article
- Mitochondria and Inflammatory Bowel Diseases: Toward a Stratified Therapeutic Intervention.Annual review of physiology · 2022Review
- Harnessing murine models of Crohn's disease ileitis to advance concepts of pathophysiology and treatment.Mucosal immunology · 2022Review
- Characterization of an intelectin-1 (Frontiers in immunology · 2022Article
- LRBA Deficiency Can Lead to Lethal Colitis That Is Diminished by SHIP1 Agonism.Frontiers in immunology · 2022Article
- Selective deletion of SHIP-1 in hematopoietic cells in mice leads to severe lung inflammation involving ILC2 cells.Scientific reports · 2021Article
- Targeting SHIP1 and SHIP2 in Cancer.Cancers · 2021Review
- Phosphatidylinositol 3-kinase p110δ drives intestinal fibrosis in SHIP deficiency.Mucosal immunology · 2019Article
- [Anti-inflammatory effect of interleukin-35 in mice with colitis and its mechanism].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2018Article
- SHIP1 Deficiency in Inflammatory Bowel Disease Is Associated With Severe Crohn's Disease and Peripheral T Cell Reduction.Frontiers in immunology · 2018Article
- RNA-seq implicates deregulation of the immune system in the pathogenesis of diverticulitis.American journal of physiology. Gastrointestinal and liver physiology · 2017Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundInflammatory 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.
aimTo determine whether SHIP plays a pivotal role in control of immune tolerance in the gut mucosa.
methodsGastrointestinal 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.
resultsSHIP-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.
conclusionsSHIP 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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.