@article{04f01ff832b349c5ac89b3f358c90471,
title = "DEFECTIVE DNA-RECEPTOR FUNCTION IN SYSTEMIC LUPUS ERYTHEMATOSUS AND RELATED DISEASES: EVIDENCE FOR AN AUTOANTIBODY INFLUENCING CELL PHYSIOLOGY",
abstract = "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.",
author = "Bennett, {R. M.} and Peller, {J. S.} and Merritt, {M. M.}",
note = "Funding Information: This work was partly supported by grants from Syntex Medical Diagnostics. Correspondence should be addressed to M. W., Department of Pediatrics JCP, University of Iowa Hospitals, Iowa City, Iowa 52242, USA. Funding Information: Foundation. R. M. B. is the recipient of a research grant from the National Institutes of Health (ROl, AM 34295-OIAI). We thank Dr Gerald Schoepflin for providing us with patient samples. Correspondence should be addressed to R. M. B., Department of Medicine (L329A), Oregon Health Sciences University, Portland, Oregon, 97201 USA. Funding Information: process is sensitive to an inhibitor of ribosomal protein translation implying that active regeneration is necessary for restoration of receptor function. These findings are consistent with the hypothesis that patients with SLE and similar disorders have leucocyte-reactive antibodies which cause accelerated degradation of the DNA receptor. Whether the reactive moiety is the DNA receptor or an associated antigen remains to be determined. This autoimmune defect appears be unique among the rheumatic disorders, since it causes a disturbance of normal cellular physiology-internalisation and degradation of DNA. Antibody-induced DNA-receptor dysfunction may be relevant to some aspects of the immunopathogenesis of SLE in terms of the cellular processing of DNA, the persistence of DNA in the circulation, and an impaired elimination of DNA/anti-DNA immune complexes. work was supported by an Arthritis Foundation Clinical Grant and a grant from the Oregon Chapter of the",
year = "1986",
month = jan,
day = "25",
doi = "10.1016/S0140-6736(86)90656-2",
language = "English (US)",
volume = "327",
pages = "186--188",
journal = "The Lancet",
issn = "0140-6736",
publisher = "Elsevier Limited",
number = "8474",
}