What is the function of integrin allb in mast cell?

整合素αIIb是一个著名的巨核细胞-血小板谱系的标志物，最近在造血祖细胞上被发现。我们现在证明整合素αIIb在小鼠和人类肥大细胞上高度表达，包括小鼠骨髓来源的肥大细胞、腹膜肥大细胞和人脐血来源的肥大细胞，并且它与细胞外基质蛋白的结合导致肥大细胞在各种刺激下的生物学功能增强。在包括FcεRI和干细胞因子的交联剂的刺激下，肥大细胞以整合素αIIb依赖的方式与细胞外基质蛋白如纤维蛋白原和von Willebrand因子黏附。此外，肥大细胞与纤维蛋白原的结合促进了细胞的增殖、细胞因子的产生和迁移，并诱导了对干细胞因子刺激的可溶性纤维蛋白原的摄取，暗示整合素αIIb参与了肥大细胞的多种功能。综上所述，小鼠和人肥大细胞表达功能性整合素αIIb。对整合素αIIb缺陷小鼠的分析表明，整合素αIIb在肥大细胞中与整合素αV竞争结合整合素β3，且整合素αIIb缺陷可减弱肥大细胞相关的过敏反应。此外，与野生型小鼠相比，整合素αIIb缺陷小鼠背部皮肤中的肥大细胞数量减少，但耳朵中的肥大细胞数量没有减少。总之，整合素αIIbβ3可能参与肥大细胞的分布和功能，但必须考虑在缺乏整合素αIIb的情况下整合素βVα3表达增强的影响。为了完全了解整合素αIIb在体内的功能，有必要进行进一步的检查，从而为肥大细胞介导性疾病带来新的治疗方法。

Integrin αIIb, a well-known marker of megakaryocyte-platelet lineage, has been recently recognized on hemopoietic progenitors. We now demonstrate that integrin αIIb is highly expressed on mouse and human mast cells including mouse bone marrow-derived mast cells, peritoneal mast cells, and human cord blood-derived mast cells, and that its binding to extracellular matrix proteins leads to enhancement of biological functions of mast cells in concert with various stimuli. With exposure to various stimuli, including cross-linking of FcεRI and stem cell factor, mast cells adhered to extracellular matrix proteins such as fibrinogen and von Willebrand factor in an integrin αIIb-dependent manner. In addition, the binding of mast cells to fibrinogen enhanced proliferation, cytokine production, and migration and induced uptake of soluble fibrinogen in response to stem cell factor stimulation, implicating integrin αIIb in a variety of mast cell functions. In conclusion, mouse and human mast cells express functional integrin αIIb.Analysis of integrin αIIb-deficient mouse delineated that integrin αIIb competed with integrin αV in associating with integrin β3 in mast cells and that mast cells-associated allergic responses were attenuated by integrin αIIb deficiency. In addition, the number of mast cells in the skin of the back, but not ear, was decreased in integrin αIIb-deficient mouse as compared with wild type mouse. Collectively, integrin αIIbβ3 might be involved in the distribution and function of mast cells, although the effect of enhanced expression levels of integrin αVβ3 in the absence of integrin αIIb must be considered. Further examination is necessary to completely understand the in vivo function of integrin αIIb, leading to new therapeutic approaches forthcoming for mast cell-mediated diseases.