Monocyte receptors for the Fc portion of IgG are increased in systemic lupus erythematosus.


Journal Article

Defective clearance of IgG-sensitized particles has been documented in systemic lupus erythematosus (SLE). This defect may be of pathogenetic significance because it allows the prolonged circulation of endogenous immune complexes with subsequent tissue deposition. To assess the possible contribution of a genetically determined defect in phagocyte Fc-IgG receptor expression or immune complex saturation of Fc-IgG receptors to impaired clearance, we used a well-characterized monomer binding assay to quantitate monocyte Fc-IgG receptors in normal controls and in 26 patients with SLE. Mean monocyte Fc-IgG receptor numbers were increased in both male and female SLE patients relative to normal controls. Increasing receptor numbers correlated positively with increasing clinical disease activity and increasing titers of antibody to native, double-stranded DNA. No significant correlation was found between any single disease symptom, organ system involvement, drug therapy, antigenic C3 levels, or immune complex levels and receptor number. A negative correlation was noted between Fc-IgG receptor binding affinity constants in SLE patients and clinical disease activity, but none of the observed affinity constants fell outside the 95% confidence normal range, and the mean affinity constants for patients both with and without active disease were not significantly different from controls. Our results are inconsistent with a genetically determined defect in Fc-IgG receptor elaboration by mononuclear phagocytes, and suggest that simple immune complex saturation does not underlie abnormal Fc-IgG-mediated clearance in SLE.

Full Text

Cited Authors

  • Fries, LF; Mullins, WW; Cho, KR; Plotz, PH; Frank, MM

Published Date

  • February 1, 1984

Published In

Volume / Issue

  • 132 / 2

Start / End Page

  • 695 - 700

PubMed ID

  • 6228597

Pubmed Central ID

  • 6228597

International Standard Serial Number (ISSN)

  • 0022-1767


  • eng

Conference Location

  • United States