Camussi G, Mencia-Huerta J M, Benveniste J
Immunology. 1977 Oct;33(4):523-34.
Immune complexes (ICs) triggered the degranulation of basophils/mastocytes in rabbit and man, thus releasing histamine and platelet-activating-factor. ICs acted upon basophils/mastocytes through complement activation and generation of anaphylatoxins and through release of cationic proteins from polymorphonuclear neutrophils. Anaphylatoxins and cationic proteins were active on human and rabbit mastocytes and on human basophils but not on rabbit basophils. Therefore, a cascade of cell to cell interactions may be envisaged implicating successively neutrophils, basophils and/or mastocytes and platelets. These interactions result in enhanced vascular permeability that allows ICs to be trapped along filtering basement membranes. This sequence could perpetuate the deposition of ICs, initially triggered by degranulation of basophils and mastocytes through the IgE-dependent mechanism, and furnish us with an explanation for the rather poorly understood involvement of platelets in immunopathology.
免疫复合物(ICs)可引发兔和人的嗜碱性粒细胞/肥大细胞脱颗粒,从而释放组胺和血小板活化因子。ICs通过补体激活和过敏毒素的产生以及通过多形核中性粒细胞释放阳离子蛋白作用于嗜碱性粒细胞/肥大细胞。过敏毒素和阳离子蛋白对人和兔的肥大细胞以及人嗜碱性粒细胞有活性,但对兔嗜碱性粒细胞无活性。因此,可以设想一系列细胞间相互作用,依次涉及中性粒细胞、嗜碱性粒细胞和/或肥大细胞以及血小板。这些相互作用导致血管通透性增强,使ICs能够沿着滤过的基底膜被困住。这一序列可能使最初由嗜碱性粒细胞和肥大细胞通过IgE依赖机制脱颗粒引发的ICs沉积持续存在,并为我们解释血小板在免疫病理学中参与程度相对难以理解的情况提供了依据。