Open AccessElevated levels of soluble interleukin‐1 receptor type II and interleukin‐1 receptor antagonist in patients with chronic arthritis: Correlations with markers of inflammation and joint destruction
Author(s) -
Jouvenne Patricia,
Vannier Edouard,
Dinarello Charles A.,
Miossec Pierre
Publication year - 1998
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/1529-0131(199806)41:6<1083::aid-art15>3.0.co;2-9
Subject(s) - interleukin 1 receptor antagonist , polyarthritis , interleukin 1 receptor , medicine , arthritis , receptor antagonist , rheumatoid arthritis , inflammation , receptor , immunology , interleukin , endocrinology , cytokine , antagonist
Objective To compare plasma levels of interleukin‐1 receptor antagonist (IL‐1Ra), soluble IL‐1 receptor type I (sIL‐1RI), and soluble IL‐1 receptor type II (sIL‐1RII) in patients with chronic polyarthritis, and to establish correlations between levels of these naturally occurring IL‐1 inhibitors and indices of disease activity and joint destruction. Methods Levels of IL‐1Ra, sIL‐1RI, and sIL‐1RII were measured in plasma samples from patients with chronic polyarthritis, using specific radioimmunoassays. Levels were correlated with indices of disease activity and joint destruction. Results Plasma levels of IL‐1Ra, sIL‐1RI, and sIL‐1RII were significantly higher in polyarthritis patients than in controls. IL‐1Ra levels correlated positively with all indices of disease activity and joint destruction ( P < 0.0001). In contrast, sIL‐1RII levels correlated negatively with indices of joint destruction, such as the Larsen score in the wrist ( P < 0.04). Interestingly, sIL‐1RII levels were higher in patients with nondestructive arthritis (Larsen score ≤1) than in patients with destructive arthritis. Levels of sIL‐1RI did not correlate with indices of disease activity or joint destruction. Conclusion The present findings indicate that increased levels of IL‐1Ra, a natural antiinflammatory acute‐phase protein, may reflect increased production and activity of IL‐1. In contrast, endogenous sIL‐1RII, unlike sIL‐1RI, may constitute a natural antiinflammatory factor in chronic polyarthritis. These differences should be taken into account when these antiinflammatory molecules are considered as prognostic markers or for therapeutic use.