Penning C A, French M A, Rowell N R, Hughes P
J Clin Lab Immunol. 1985 Jul;17(3):125-30.
Sera from 35 patients with systemic lupus erythematosus were examined for a cytotoxic effect on human umbilical vein endothelium. Although none of these sera produced direct cytotoxicity of 51Cr-labelled endothelial cells, even with added complement, 3 sera regularly produced increased 51Cr release when co-cultured with endothelial cells and normal human peripheral blood mononuclear cells. The effector cells involved in this cytotoxicity possessed Fc-receptors but were non-T and non-adherent while fractionation studies indicated that the responsible serum factor(s) was IgG, probably in the form of immune complexes of small size. Control studies, using sera from both 27 normal controls and 19 patients with either diabetes or extensive atherosclerotic vascular disease failed to reveal any similar cytotoxicity. Two of the 3 patients, whose sera produced this antibody-dependent cellular cytotoxicity, had had clinical episodes of major vascular thrombosis, raising the possibility that the cytotoxicity might provide an additional pathogenic mechanism in certain patients with systemic lupus erythematosus.
检测了35例系统性红斑狼疮患者血清对人脐静脉内皮细胞的细胞毒性作用。尽管这些血清中没有一种能产生对51Cr标记的内皮细胞的直接细胞毒性，即使加入补体也是如此，但有3份血清在与内皮细胞和正常人外周血单个核细胞共培养时，能使51Cr释放量持续增加。参与这种细胞毒性作用的效应细胞具有Fc受体，但不是T细胞且不黏附，而分级分离研究表明，起作用的血清因子是IgG，可能是以小尺寸免疫复合物的形式存在。使用27名正常对照者以及19例糖尿病患者或广泛动脉粥样硬化性血管疾病患者的血清进行的对照研究，均未发现任何类似的细胞毒性。其血清产生这种抗体依赖性细胞毒性的3例患者中有2例曾发生过严重血管血栓形成的临床发作，这增加了细胞毒性可能为某些系统性红斑狼疮患者提供额外致病机制的可能性。
