Hashimoto Y, Nakano K, Yoshinoya S, Tanimoto K, Itoh K
Department of Internal Medicine & Physical Therapy, University of Tokyo School of Medicine, Japan.
Scand J Rheumatol. 1992;21(5):209-14. doi: 10.3109/03009749209099226.
When normal polymorphonuclear leukocytes (PMN) were incubated with sera from patients with active systemic lupus erythematosus (SLE), a significantly increased cytotoxicity against human cultured vascular endothelial cells (EC), compared with normal control sera, was demonstrated by the standard 51Cr release method. The degree of this cytotoxicity was correlated with the immune complex level in each serum. The cytotoxicity did not correlate with the presence of anti-EC antibody. An absorption study with C1q-Sepharose 4B further suggested that the immune complexes are the factor which induce cytotoxicity. A gel fractionation study, however, indicated the heterogenity of the cytotoxic activity, and suggested the possible contribution of other substances including anti-EC, at least in some of the patients. This type of cytotoxicity may initiate the inflammatory process including vascular damage of the disease.
当正常多形核白细胞(PMN)与活动性系统性红斑狼疮(SLE)患者的血清一起孵育时,通过标准的51Cr释放法证明,与正常对照血清相比,其对人培养的血管内皮细胞(EC)的细胞毒性显著增加。这种细胞毒性的程度与每种血清中的免疫复合物水平相关。细胞毒性与抗EC抗体的存在无关。用C1q-琼脂糖凝胶4B进行的吸收研究进一步表明,免疫复合物是诱导细胞毒性的因素。然而,凝胶分级分离研究表明细胞毒性活性具有异质性,并提示至少在一些患者中,包括抗EC在内的其他物质可能也有作用。这种类型的细胞毒性可能引发包括该疾病血管损伤在内的炎症过程。