Bogman M J, Berden J H, Cornelissen I M, Maass C N, Koene R A
Am J Pathol. 1982 Oct;109(1):97-106.
Rat skin grafts carried by immunosuppressed mice can be acutely destroyed by intravenous administration of mouse anti-rat antibody. The velocity of the reaction and the histologic sequence of events depend on the amount of antibody administered: low doses give an Arthus-like rejection, whereas at high doses a Shwartzman-like pattern occurs. Depletion of C3 by cobra venom factor treatment did not prevent acute rejection after intravenous injection of high doses of antiserum but changed the reaction from a Shwartzman-like to an Arthus-like pattern. Conversely, supplementary administration of rabbit complement caused a violent Shwartzman-like graft destruction after injection of low doses of antibody, which in complement-normal mice gave an Arthus-like reaction. The results show that complement can greatly amplify the antibody-mediated immune vasculitis and can substantially modify its histologic pattern. It is, however, not an absolute requirement for the occurrence of the destructive process.
免疫抑制小鼠携带的大鼠皮肤移植物,可通过静脉注射小鼠抗大鼠抗体而被急性破坏。反应的速度和组织学事件序列取决于所给予抗体的量:低剂量会产生类似阿瑟斯反应的排斥,而高剂量时则出现类似施瓦茨曼反应的模式。用眼镜蛇毒因子处理使C3耗竭,在静脉注射高剂量抗血清后并不能防止急性排斥,但会使反应从类似施瓦茨曼反应的模式转变为类似阿瑟斯反应的模式。相反,补充给予兔补体,在注射低剂量抗体后会导致剧烈的类似施瓦茨曼反应的移植物破坏,而在补体正常的小鼠中这会产生类似阿瑟斯反应。结果表明,补体可极大地放大抗体介导的免疫性血管炎,并可实质性地改变其组织学模式。然而,对于破坏性过程的发生,补体并非绝对必需。