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Published on: January 29, 2014
Serum COMP-C3b complexes in rheumatic diseases and relation to anti-TNF-α treatment
Kaisa E Happonen1, Tore Saxne, Pierre Geborek
1Department of Laboratory Medicine Malmö, Section of Medical Protein Chemistry, Lund University, Wallenberg Laboratory floor 4, SE-205 02 Malmö, Sweden.
Insights
Cartilage oligomeric matrix protein-C3b (COMP-C3b) complexes are elevated in various joint diseases, including rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). COMP-C3b levels correlate with RA disease activity and change with TNF-α inhibitor treatment.
Area of Science:
- Rheumatology
- Immunology
- Biochemistry
Background:
- Cartilage oligomeric matrix protein (COMP) is elevated in joint diseases like rheumatoid arthritis (RA) and osteoarthritis (OA).
- COMP activates the complement system's alternative pathway, forming COMP-C3b complexes found in RA patients' sera.
Purpose of the Study:
- To investigate COMP-C3b levels in larger patient cohorts across various rheumatologic diseases.
- To explore the clinical significance and disease correlations of COMP-C3b as a potential biomarker.
Main Methods:
- Serum COMP-C3b levels were quantified using an enzyme-linked immunosorbent assay (ELISA).
- Serum COMP levels were also measured via ELISA.
Main Results:
- COMP-C3b was significantly elevated in RA, systemic lupus erythematosus (SLE), ankylosing spondylitis (AS), psoriatic arthritis (PsA), and osteoarthritis (OA).
- COMP-C3b levels correlated with disease activity in RA and showed distinct changes during anti-tumor necrosis factor (TNF)-α therapy compared to C-reactive protein (CRP).
- COMP-C3b levels did not correlate with COMP levels in any patient group.
Conclusions:
- COMP-C3b serves as a valuable biomarker elevated across multiple inflammatory rheumatologic conditions.
- COMP-C3b dynamics during anti-TNF-α therapy suggest it reflects disease-specific features beyond general inflammation markers like CRP.
Introduction:
Cartilage oligomeric matrix protein (COMP) is found at elevated concentrations in sera of patients with joint diseases such as rheumatoid arthritis (RA) and osteoarthritis (OA). We recently showed that COMP activates complement via the alternative pathway and that COMP-C3b complexes are present in sera of RA patients, but not in healthy controls. We now set out to elaborate on the information provided by this marker in a variety of diseases and larger patient cohorts.
Methods:
COMP-C3b levels in sera were measured by using an enzyme-linked immunosorbent assay (ELISA) capturing COMP and detecting C3b. Serum COMP was measured by using ELISA.
Results:
COMP-C3b levels were significantly elevated in patients with RA as well as in systemic lupus erythematosus (SLE), compared with healthy controls. SLE patients with arthritis had significantly higher COMP-C3b levels than did those without. COMP-C3b was furthermore elevated in patients with ankylosing spondylitis (AS), psoriatic arthritis (PsA), reactive arthritis, systemic sclerosis, and OA. COMP-C3b did not correlate with COMP in any of the patient groups. COMP-C3b correlated with disease activity in RA, but not in other diseases. COMP-C3b levels in RA patients decreased on treatment with tumor necrosis factor (TNF)-α inhibitors, whereas the levels increased in patients with AS or PsA. The changes of COMP-C3b did not parallel the changes of C-reactive protein (CRP).
Conclusions:
COMP-C3b levels are elevated in several rheumatologic diseases and correlate with inflammatory measures in RA. COMP-C3b levels in RA decrease during TNF-α inhibition differently from those of CRP, suggesting that formation of COMP-C3b relates to disease features not reflected by general inflammation measures.
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