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Autoantibodies against granulocyte−macrophage colony stimulating factor and interleukin-3 are rare in patients with Felty’s syndrome
  1. B Hellmich1,*,
  2. A Ciaglo1,
  3. H Schatz1,
  4. G Coakley2,
  1. 1Medizinische Klinik und Poliklinik, BG Kliniken Bergmannsheil, Universitätsklinikum der Ruhr-Universität Bochum, Bürckle-de-la-Camp-Platz 1, Bochum, Germany
  2. 2Department of Rheumatology, Guy’s, King’s and St. Thomas Hospitals School of Medicine, London SE1 9RT, UK
  1. Correspondence to:
    Dr B Hellmich
    Poliklinik für Rheumatologie, Universitätsklinikum Schleswig-Holstein, Campus Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany; hellmichrheuma-zentrum.de

Abstract

Objectives: Antibodies against granulocyte colony stimulating factor are frequently found in patients with Felty’s syndrome (FS). In this study, we examined the prevalence of antibodies against two other granulopoietic cytokines: granulocyte−macrophage colony stimulating factor (GM-CSF) and interleukin-3 (IL3).

Methods: Sera of 32 patients with FS, 20 normocytic patients with rheumatoid arthritis (RA), and 72 healthy individuals were screened for the presence of antibodies against GM-CSF and IL3 by ELISA and bioassays, using the human erythroleukaemia cell line TF-1.

Results: In two of the 32 patients with FS, antibodies to GM-CSF and IL3 were detectable by ELISA. Binding anti-GM-CSF antibodies were also detected in one of the 72 healthy controls, while in another healthy subject and in one of the patients with normocytic RA, anti-IL3 antibodies were present. Serum from one of the two patients with FS who tested positive for anti-IL3 and anti-GM-CSF antibodies by ELISA showed strong neutralising capacity to the biological effect of IL3, but not to GM-CSF in vitro. Patients with FS had significantly higher serum levels of GM-CSF (median; 2.82 pg/mL; interquartile range 2.64–3.19 pg/mL) compared with patients with RA (2.52 pg/mL; 2.28–2.72 pg/mL; p = 0.012) and healthy controls (2.23 pg/mL; 2.04–2.52; p<0.001). In addition, serum levels of IL3 in patients were significantly higher in FS (10.05 pg/mL; 8.94–11.98) compared with controls (4.79 pg/mL; 3.72–7.22; p<0.001), but not compared with RA patients (9.52 pg/mL; 8.32–10.42; p = 0.17).

Conclusions: Antibodies to GM-CSF and IL3 are rare in patients with FS and RA and in healthy subjects. In individual patients with FS, the presence of neutralising anti-IL3 antibodies may contribute to the development of cytopenia.

  • ANC, absolute neutrophil count
  • FS, Felty’s syndrome
  • G-CSF, granulocyte colony stimulating factor
  • GM-CSF, granulocyte−macrophage colony stimulating factor
  • IL3, interleukin-3
  • LGL, large granular lymphocytes
  • RA, rheumatoid arthritis
  • RF, rheumatoid factor
  • rh, recombinant human
  • Felty’s syndrome
  • anti-GM-CSF antibodies
  • anti-IL3 antibodies
  • granulocyte−macrophage colony stimulating factor
  • interleukin-3

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Footnotes

  • * Present address: Poliklinik für Rheumatologie, Universitätsklinikum Schleswig-Holstein, Campus Lübeck, Lübeck, Germany

  • Present address: Department of Rheumatology, Queen Elizabeth Hospital, Stadium Road, London SE18 4QH, UK

  • Competing interests: none declared