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特异的IgE抗体结合予肥大细胞和嗜碱细胞的表面,和相应的抗原相接触,由浆细胞释放出影响血管的胺类和一种亲嗜伊红细胞因子。基本与两个相邻近抗体在同一细胞上和二价染色体接触而形成的一个桥相似。这个在抗体FC处的变化和细胞表面形状的改变被认为是腺嘌呤环烷活性的干扰。腺苷环烷系一种能转变三磷酸腺苷(ATP)为环磷酸腺苷(环—AmP)的酶,而环～AmP为维持细胞颗粒的稳定所必须。故腺苷环烷的任何减少,将导致组织胺和其他药物活性因素的释放。值得注意的是,无论是活化性腺苷环烷(eg肾上腺素)还是抑制性磷酸二脂酶,任何增加肥大细胞环单磷酸腺苷水平的
Specific IgE antibodies bind to the surface of mast cells and basophils and come into contact with the corresponding antigens, releasing plasma-affecting amines and a pro-eosinophil. Basically similar to the formation of a bridge between two adjacent antibodies on the same cell as the bivalent chromosome. This change at the antibody FC and the change of the cell surface shape is considered to be an interference of the adenine naphthenic activity. Adenycloalkane is an enzyme that converts adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cyclo-AmP), whereas loop AmP is necessary to maintain cell particle stability. Therefore, any reduction of adenosine ring will result in the release of histamine and other pharmacologically active agents. It is noteworthy that, whether activated adenosine cycloalkane (eg epinephrine) or inhibit phosphodiesterase, any increase in mast cell loop adenosine monophosphate