{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T22:52:07Z","timestamp":1788821527203,"version":"build-2803163510"},"reference-count":43,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2009,7,1]],"date-time":"2009-07-01T00:00:00Z","timestamp":1246406400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2009,7,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>SHIP1 inhibits immune receptor signaling through hydrolysis of the PI3K product phosphatidylinositol 3,4,5-trisphosphate, forming phosphatidylinositol 3,4-bisphosphate. In mast cells, SHIP1 represses Fc\u03b5RI- and cytokine-mediated activation in vitro, but little is known regarding the function of SHIP1 in mast cells in vivo or the susceptibility of Ship1\u2212\/\u2212 mice to mast cell-associated diseases. In this study, we found that Ship1\u2212\/\u2212 mice have systemic mast cell hyperplasia, increased serum levels of IL-6, TNF, and IL-5, and heightened anaphylactic response. Further, by reconstituting mast cell-deficient mice with Ship1+\/+ or Ship1\u2212\/\u2212 mast cells, we found that the above defects were due to loss of SHIP1 in mast cells. Additionally, we found that mice reconstituted with Ship1\u2212\/\u2212 mast cells suffered worse allergic asthma pathology than those reconstituted with Ship1+\/+ mast cells. In summary, our data show that SHIP1 represses allergic inflammation and mast cell hyperplasia in vivo and exerts these effects specifically in mast cells.<\/jats:p>","DOI":"10.4049\/jimmunol.0900427","type":"journal-article","created":{"date-parts":[[2009,6,19]],"date-time":"2009-06-19T17:04:08Z","timestamp":1245431048000},"page":"228-236","source":"Crossref","is-referenced-by-count":50,"title":["SHIP1 Is a Repressor of Mast Cell Hyperplasia, Cytokine Production, and Allergic Inflammation In Vivo"],"prefix":"10.1093","volume":"183","author":[{"given":"D James","family":"Haddon","sequence":"first","affiliation":[{"name":"The Biomedical Research Centre"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frann","family":"Antignano","sequence":"additional","affiliation":[{"name":"Terry Fox Laboratory, University of British Columbia , Vancouver, British Columbia,","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael R","family":"Hughes","sequence":"additional","affiliation":[{"name":"The Biomedical Research Centre"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marie-Ren\u00e9e","family":"Blanchet","sequence":"additional","affiliation":[{"name":"The Biomedical Research Centre"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lori","family":"Zbytnuik","sequence":"additional","affiliation":[{"name":"The Biomedical Research Centre"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gerald","family":"Krystal","sequence":"additional","affiliation":[{"name":"Terry Fox Laboratory, University of British Columbia , Vancouver, British Columbia,","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kelly M","family":"McNagny","sequence":"additional","affiliation":[{"name":"The Biomedical Research Centre"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2009,7,1]]},"reference":[{"key":"2026012811285777000_R1","first-page":"11382","article-title":"T cell-specific deletion of the inositol phosphatase SHIP reveals its role in regulating Th1\/Th2 and cytotoxic responses.","volume-title":"Proc. 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