Interleukin-1-inhibitory IgG in sera from some patients with rheumatoid arthritis

Arthritis Rheum. 1989 Dec;32(12):1528-38. doi: 10.1002/anr.1780321206.


Inhibition of interleukin-1 alpha (IL-1 alpha) activity was detected in 7 of 41 serum samples from patients with rheumatoid arthritis (RA). These 7 sera inhibited not only IL-1 alpha-induced endothelial cell adherence to neutrophils, but also IL-1 beta-induced endothelial cell adherence, although to a lesser extent. These sera showed no influence on tumor necrosis factor-induced endothelial cell adherence. No inhibitory activity was found in 40 sera from normal control subjects. Studies to further examine these effects included gel filtration analysis of 2 of the RA sera. The inhibitory activity was eluted near Mr 158 kd and above Mr 250 kd. Analysis by protein A affinity chromatography showed that IL-1-inhibitory activity was present in protein A-binding fractions. Purified IgG (by DE-52 column chromatography) from RA patients was found to be as potent an inhibitor as the protein A-binding fractions, which suggests that the major inhibitory activity in RA sera is attributable to IgG molecules. These purified IgG molecules also inhibited IL-1-induced proliferation of mouse thymocytes but did not influence IL-2-dependent proliferation of the CTLL-2 murine T cell line. The 7 patients whose sera showed IL-1-inhibitory activity had mild RA and low titers of rheumatoid factor. The findings, taken together, suggest a possible regulatory role of IL-1-inhibitory IgG in RA disease activity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Animals
  • Arthritis, Rheumatoid / blood*
  • Cell Adhesion / drug effects
  • Cell Division / drug effects
  • Endothelium, Vascular / cytology
  • Endothelium, Vascular / drug effects
  • Female
  • Humans
  • Immunoglobulin G / isolation & purification
  • Immunoglobulin G / physiology*
  • Interleukin-1 / antagonists & inhibitors*
  • Interleukin-1 / pharmacology
  • Male
  • Mice
  • Middle Aged
  • Neutrophils / physiology
  • Reference Values
  • Rheumatoid Factor / analysis
  • Thymus Gland / cytology
  • alpha 1-Antitrypsin / analysis


  • Immunoglobulin G
  • Interleukin-1
  • alpha 1-Antitrypsin
  • Rheumatoid Factor