Endothelial cell destruction by polymorphonuclear leukocytes incubated with sera from patients with systemic lupus erythematosus (SLE).
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.
Hashimoto
Y
Y
Department of Internal Medicine & Physical Therapy, University of Tokyo School of Medicine, Japan.
Nakano
K
K
Yoshinoya
S
S
Tanimoto
K
K
Itoh
K
K
D000328:Adult; D000911:Antibodies, Monoclonal; D000936:Antigen-Antibody Complex / Q000032:analysis; D016923:Cell Death / Q000502:physiology; D002458:Cell Fractionation; D002478:Cells, Cultured; D002850:Chromatography, Gel; D003176:Complement C3 / Q000032:analysis; D003602:Cytotoxicity, Immunologic; D004730:Endothelium, Vascular / Q000276:immunology / Q000473:pathology*; D005260:Female; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D009504:Neutrophils / Q000473:pathology* / Q000502:physiology
D000911:Antibodies, Monoclonal; D000936:Antigen-Antibody Complex; D003176:Complement C3