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Macrophage activity assessed by soluble CD163 in early rheumatoid arthritis: association with disease activity but
Stinne Ravn Greisen1, Holger Jon Møller2, Kristian Stengaard-Pedersen3
1Department of Biomedicine, Aarhus University; and Department of Rheumatology, Aarhus University Hospital, Denmark.
Objectives:
Rheumatoid arthritis (RA) is a chronic autoimmune disease where TNF-α is a central mediator of inflammation, and is cleaved from the cell surface by TACE/ADAM17. This metalloproteinase is also responsible for the release of soluble (s) CD163. Soluble CD163 reflects macrophage activation. In RA, sCD163 has been suggested as a marker of disease activity and progression. Our aim is to investigate sCD163 levels in early RA patients.
Methods:
Soluble CD163 was measured by ELISA from 150 RA plasma samples from the OPERA trial. Averaged disease duration was three months, prior to randomisation with methotrexate (MTX) and adalimumab (DMARD+ADA) or MTX and placebo (DMARD+PLA). Soluble CD163 levels were evaluated in relation to clinical disease parameters.
Results:
Plasma sCD163 at baseline was 2.39 mg/l (1.74 mg/l-3.18 mg/l), mean (95% CI), vs healthy controls: 1.63 mg/l (1.54 mg/l - 1.73 mg/l), (p<0.001). After three months of treatment sCD163 levels decreased significantly (average 23.5%) in both treatment groups. Significant incremental sCD163 levels followed withdrawal of ADA after 12 months of treatment. Baseline sCD163 correlated with CRP and all investigated disease activity markers (ρ=0.16-0.28, p<0.05). In the DMARD+PLA group baseline sCD163 also correlated with CRP during the follow-up period.
Conclusions:
Soluble CD163 correlated with disease activity markers in early RA before treatment. Plasma sCD163 may add to currently available disease measures by specifically reflecting changes in macrophage activity as evidenced by increasing levels following anti-TNF withdrawal, despite maintenance of a stable clinical condition achieved by conventional remedies. It remains to be determined whether sCD163 is an early predictor of disease flare.
Insights
Soluble CD163 levels are elevated in early rheumatoid arthritis (RA) and correlate with disease activity. These levels decrease with treatment but rise upon anti-TNF withdrawal, suggesting sCD163 reflects macrophage activity in RA.
Area of Science:
- Immunology
- Rheumatology
- Biochemistry
Background:
- Rheumatoid arthritis (RA) is a chronic autoimmune disease driven by inflammation, with TNF-α as a key mediator.
- Tumor necrosis factor-α-converting enzyme (TACE/ADAM17) cleaves cell-surface TNF-α and releases soluble CD163 (sCD163).
- Soluble CD163 is a marker of macrophage activation, potentially indicating RA disease activity and progression.
Purpose of the Study:
- To investigate soluble CD163 (sCD163) levels in patients with early rheumatoid arthritis (RA).
- To evaluate the relationship between sCD163 levels and clinical disease parameters in early RA.
- To assess the utility of sCD163 as a marker of macrophage activity in RA.
Main Methods:
- Plasma samples from 150 early RA patients in the OPERA trial were analyzed using ELISA for sCD163.
- Patients had an average disease duration of three months before randomization to methotrexate (MTX) with adalimumab (DMARD+ADA) or placebo (DMARD+PLA).
- sCD163 levels were assessed at baseline and after three months of treatment, with follow-up after 12 months for some patients.
Main Results:
- Baseline plasma sCD163 levels were significantly higher in RA patients (2.39 mg/l) compared to healthy controls (1.63 mg/l).
- sCD163 levels decreased by an average of 23.5% after three months of treatment in both RA treatment groups.
- Increased sCD163 levels were observed after adalimumab withdrawal, and baseline sCD163 correlated with CRP and other disease activity markers.
Conclusions:
- Soluble CD163 levels correlate with disease activity markers in early RA patients before treatment.
- Plasma sCD163 may offer additional insights into disease measures by reflecting macrophage activity changes.
- Rising sCD163 levels after anti-TNF withdrawal suggest its potential as a specific indicator of macrophage response in RA.
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