DEFECTIVE DNA-RECEPTOR FUNCTION IN SYSTEMIC LUPUS ERYTHEMATOSUS AND RELATED DISEASES: EVIDENCE FOR AN AUTOANTIBODY INFLUENCING CELL PHYSIOLOGY

R. M. Bennett, J. S. Peller, M. M. Merritt

Research output: Contribution to journalArticlepeer-review

25 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)186-188
Number of pages3
JournalThe Lancet
Volume327
Issue number8474
DOIs
StatePublished - Jan 25 1986
Externally publishedYes

ASJC Scopus subject areas

  • Medicine(all)

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