Upregulation of cytokine receptors sTNF-R55, sTNF-R75, and sIL-2R in psoriatic arthritis synovial fluid

J Rheumatol. 1998 Jan;25(1):105-10.

Abstract

Objective: To assess differences in soluble tumor necrosis factor receptor 55 (sTNF-R55), sTNF-R75, and soluble interleukin 2 receptor (sIL-2R) in synovial fluid (SF) of patients with psoriatic arthritis (PsA), a seronegative inflammatory joint disease, in comparison with those of patients with rheumatoid arthiritis (RA) and osteoarthritis (OA).

Methods: sIL-R were measured in SF with commercial sandwich ELISA and the results correlated with serological and clinical disease activity variables.

Results: In PsA SF the level of sTNF-R55 was 11.8 +/- 0.8 ng/ml and that of sTNF-R75 13.0 +/- 1.3 ng/ml. sIL-2R concentration in PsA SF was 800 +/- 84 U/ml. Compared to PsA SF, cytokine receptor levels in OA SF were significantly lower: 8.7 +/- 0.8 ng/ml for sTNF-R55 (p < 0.02); 7.1 +/- 0.9 ng/ml for sTNF-R75 (p < 0.0003); and 505 +/- 53 U/ml for sIL-2R (p < 0.009). In contrast RA SF cytokine receptor levels were even higher than those of PsA SF (sTNF-R55: 18.1 +/- 2.0 ng/ml, p < 0.04; sTNF-R75: 29.5 +/- 2.9 ng/ml, p < 0.0002; and for sIL-2R: 1957 +/- 290 U/ml, p < 0.03).

Conclusion: In PsA SF sTNF-R55, sTNF-R75, and sIL-2R are upregulated compared to OA SF but are lower than in RA SF. Our results for TNF-R agree with recent findings in PsA, since TNF-alpha, an important stimulator for TNF-R, is also significantly lower in PsA than in RA. The upregulation of the cytokine receptors in PsA reconfirms its inflammatory nature, but indicates the more benign course of disease compared with RA.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Arthritis, Psoriatic / metabolism*
  • Arthritis, Rheumatoid / metabolism
  • Humans
  • Middle Aged
  • Osteoarthritis / metabolism
  • Receptors, Interleukin-2 / metabolism*
  • Receptors, Tumor Necrosis Factor / metabolism*
  • Synovial Fluid / metabolism*
  • Tumor Necrosis Factor-alpha / metabolism
  • Up-Regulation

Substances

  • Receptors, Interleukin-2
  • Receptors, Tumor Necrosis Factor
  • Tumor Necrosis Factor-alpha