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Updated: Feb 28, 2026

Single-cell Analysis of Immunophenotype and Cytokine Production in Peripheral Whole Blood via Mass Cytometry
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Soluble CD206 plasma levels in rheumatoid arthritis reflect decrease in disease activity.

Line Dam Heftdal1, Kristian Stengaard-Pedersen2, Lykke Midtbøll Ørnbjerg3

  • 1a Department of Biomedicine , Aarhus University , Aarhus , Denmark.

Scandinavian Journal of Clinical and Laboratory Investigation
|June 10, 2017
PubMed
Summary

Soluble CD206 (sCD206) levels in early rheumatoid arthritis (RA) patients decreased with treatment. Anti-TNFα therapy maintained lower sCD206 levels, suggesting its role in M2 macrophage activity during RA.

Keywords:
Cluster of differentiation 206macrophagesmannose-binding lectinrheumatoid arthritistumor necrosis factor-alpha

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Area of Science:

  • Immunology
  • Rheumatology
  • Biochemistry

Background:

  • Rheumatoid arthritis (RA) involves chronic joint inflammation driven by activated macrophages.
  • Tumor Necrosis Factor alpha (TNFα) is a key mediator in RA pathogenesis.
  • The mannose receptor CD206, expressed on M2 macrophages, is involved in collagen processing, and its soluble form (sCD206) may indicate M2 macrophage activation.

Purpose of the Study:

  • To investigate plasma levels of soluble CD206 (sCD206) in early rheumatoid arthritis (RA) patients starting anti-TNFα therapy.
  • To assess the relationship between sCD206 levels, disease activity, and treatment response in early RA.

Main Methods:

  • Plasma sCD206 levels were measured using ELISA in 155 early RA patients.
  • Patients received methotrexate with either placebo or adalimumab (anti-TNFα) for 12 months, followed by open-label treatment.
  • Disease activity was assessed over 24 months.

Main Results:

  • Baseline sCD206 levels in treatment-naïve RA patients were at the upper limit of the healthy reference range.
  • In the placebo group, sCD206 decreased initially but returned to baseline by 6 months.
  • Adalimumab treatment group showed sustained lower sCD206 levels compared to baseline throughout the study.

Conclusions:

  • Plasma sCD206 levels in early RA decrease with disease activity and DMARD initiation.
  • Anti-TNFα therapy, specifically adalimumab, effectively maintained the reduction in sCD206 levels.
  • sCD206 shows potential as a biomarker for M2 macrophage activity in RA patients undergoing anti-TNFα treatment.