Tam See-Ying, Tsai Mindy, Snouwaert John N, Kalesnikoff Janet, Scherrer Didier, Nakae Susumu, Chatterjea Devavani, Bouley Donna M, Galli Stephen J
Department of Pathology, Stanford University School of Medicine, Stanford, California 94305, USA.
Nat Immunol. 2004 Aug;5(8):844-52. doi: 10.1038/ni1093. Epub 2004 Jul 4.
Mast cell activation induced by aggregation of Fc epsilon RI receptors with immunoglobulin E and antigen is mediated through the activation of multiple protein kinase cascades. Here we report that the regulatory protein RabGEF1 bound to Ras and negatively regulated Ras activation and its 'downstream' effector pathways in Fc epsilon RI-dependent mast cell activation. RabGEF1-deficient mast cells showed enhanced degranulation and release of lipid mediators and cytokines in response to Fc epsilon RI aggregation. RabGEF1-deficient mice developed severe skin inflammation and had increased numbers of mast cells. Thus, RabGEF1 is a negative regulator of Fc epsilon RI-dependent mast cell activation, and a lack of RabGEF1 results in the development of skin inflammation in vivo.
由FcεRI受体与免疫球蛋白E和抗原聚集诱导的肥大细胞活化是通过多种蛋白激酶级联反应的激活介导的。在此,我们报告调节蛋白RabGEF1与Ras结合,并在FcεRI依赖性肥大细胞活化中负向调节Ras活化及其“下游”效应途径。RabGEF1缺陷型肥大细胞在FcεRI聚集时表现出增强的脱颗粒以及脂质介质和细胞因子的释放。RabGEF1缺陷型小鼠出现严重的皮肤炎症,且肥大细胞数量增加。因此,RabGEF1是FcεRI依赖性肥大细胞活化的负调节因子,缺乏RabGEF1会导致体内皮肤炎症的发生。