Henson P M, Cochrane C G
J Exp Med. 1971 Mar 1;133(3):554-71. doi: 10.1084/jem.133.3.554.
By depletion of C3 from rabbits undergoing acute experimental immune complex disease with an anticomplementary factor in cobra venom, it has been possible to demonstrate that deposition of the complexes in arteries and glomeruli does not require the complement components reacting after C2. Immunological reactions, in which platelets release their vasoactive amines, have been examined in rabbits undergoing immune complex disease. A correlation was obtained between the presence of a complement-independent reaction which required blood leukocytes, antigen and platelets, the deposition of immune complexes, and the induction of glomerulonephritis. C3 depletion did, however, have a marked alleviating effect on the severity of the arterial lesions. Neutrophil accumulation and the subsequent necrotizing arteritis were prevented. In contrast, the character and severity of the glomerulonephritis was not altered by depletion of later-acting complement components.
通过用眼镜蛇毒中的抗补体因子使患有急性实验性免疫复合物疾病的兔子体内的C3耗竭，已能够证明复合物在动脉和肾小球中的沉积不需要C2之后起反应的补体成分。在患有免疫复合物疾病的兔子中，对血小板释放其血管活性胺的免疫反应进行了研究。在一种需要血液白细胞、抗原和血小板的不依赖补体的反应的存在、免疫复合物的沉积与肾小球肾炎的诱发之间获得了相关性。然而，C3耗竭对动脉病变的严重程度有显著的缓解作用。阻止了中性粒细胞聚集和随后的坏死性动脉炎。相比之下，后期起作用的补体成分的耗竭并未改变肾小球肾炎的特征和严重程度。
