| First Author | Haddon DJ | Year | 2009 |
| Journal | J Immunol | Volume | 183 |
| Issue | 1 | Pages | 228-36 |
| PubMed ID | 19542434 | Mgi Jnum | J:149977 |
| Mgi Id | MGI:3849502 | Doi | 10.4049/jimmunol.0900427 |
| Citation | Haddon DJ, et al. (2009) SHIP1 Is a repressor of mast cell hyperplasia, cytokine production, and allergic inflammation in vivo. J Immunol 183(1):228-36 |
| abstractText | 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 FcepsilonRI- 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(-/-) mice to mast cell-associated diseases. In this study, we found that Ship1(-/-) 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(-/-) 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(-/-) 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. |
