Haddon D James, Antignano Frann, Hughes Michael R, Blanchet Marie-Renée, Zbytnuik Lori, Krystal Gerald, McNagny Kelly M
The Biomedical Research Centre, University of British Columbia, Vancouver, Canada.
J Immunol. 2009 Jul 1;183(1):228-36. doi: 10.4049/jimmunol.0900427.
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.
SHIP1通过水解PI3K产物磷脂酰肌醇3,4,5-三磷酸形成磷脂酰肌醇3,4-二磷酸来抑制免疫受体信号传导。在肥大细胞中,SHIP1在体外可抑制FcepsilonRI和细胞因子介导的激活,但SHIP1在体内肥大细胞中的功能或Ship1(-/-)小鼠对肥大细胞相关疾病的易感性尚不清楚。在本研究中,我们发现Ship1(-/-)小鼠存在全身性肥大细胞增生、血清IL-6、TNF和IL-5水平升高以及过敏反应增强。此外,通过用Ship1(+/+)或Ship1(-/-)肥大细胞重建肥大细胞缺陷小鼠,我们发现上述缺陷是由于肥大细胞中SHIP1的缺失所致。此外,我们发现用Ship1(-/-)肥大细胞重建的小鼠比用Ship1(+/+)肥大细胞重建的小鼠患有更严重的过敏性哮喘病理。总之,我们的数据表明SHIP1在体内抑制过敏性炎症和肥大细胞增生,并在肥大细胞中特异性发挥这些作用。