Defective DNA-receptor function in systemic lupus erythematosus and related diseases: evidence for an autoantibody influencing cell physiology.
The receptor for DNA was functionally defective in the majority of patients with systemic lupus erythematosus (SLE; 91% of 35 studied) and allied rheumatic disorders. This functional defect was manifest by impaired binding of exogenous DNA to the cell surface of peripheral blood mononuclear cells and an inability of cells to internalise and degrade DNA. The receptor defect was not constitutive, since it could be reversed by overnight incubation of cells; this process was sensitive to cycloheximide, suggesting a requirement for active receptor regeneration. The DNA-receptor defect could be induced in healthy controls, by incubating their cells with the serum of patients with SLE. The humoral factor inducing the defect was an autoantibody.
Bennett
R M
RM
Peller
J S
JS
Merritt
M M
MM
D001323:Autoantibodies / Q000032:analysis*; D001667:Binding, Competitive; D002478:Cells, Cultured; D003513:Cycloheximide / Q000494:pharmacology; D004247:DNA / Q000378:metabolism; D006801:Humans; D007128:Immunoglobulin Fragments / Q000032:analysis; D007074:Immunoglobulin G / Q000276:immunology; D008180:Lupus Erythematosus, Systemic / Q000276:immunology* / Q000378:metabolism; D011956:Receptors, Cell Surface / Q000276:immunology* / Q000378:metabolism; D012214:Rheumatic Heart Disease / Q000276:immunology / Q000378:metabolism; D014316:Tritium
D001323:Autoantibodies; C033365:DNA receptor; D007128:Immunoglobulin Fragments; D007074:Immunoglobulin G; D011956:Receptors, Cell Surface; D014316:Tritium; D004247:DNA; D003513:Cycloheximide