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SHIP deficiency causes Crohn's disease-like ileitis
Inflammatory bowel disease is characterised by changes in intestinal epithelial cell integrity and immune regulation. SHIP controls the homeostasis of immunoregulatory myeloid and T lymphoid cells. In this study, the authors determined if SHIP plays a role in control of immune tolerance in the gut mucosa. They studied SHIP deficient mice and their respective wild-type (WT) littermates. To determine if SHIP is needed for intestinal epithelial barrier integrity or mucosal immunoregulation, SHIP-deficient hosts were reconstituted with WT haematopoietic cell grafts, and WT hosts with SHIP-deficient haematopoietic grafts including whole splenocytes, purified T cells or NK cells. The results of these experiments show that SHIP-deficient mice develop segmental, transmural pyogranulomatous ilietis resembling the changes observed in Crohn's disease (see figure). WT Bone marrow reconstitution of SHIP-/- hosts corrected ileitis and reconstitution with SHIP-/- splenocytes transferred ileitis to WT hosts. They conclude that SHIP plays a pivotal role in immune function in the intestine and that further study in IBD is required. Also, SHIP-deficient ileitis results from a local deficit in mucosal T cell immunity that promotes a damaging granulocyte-monocyte inflammation of the distal ileum. See page 177.
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