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OP0236 Elevated Soluble CD163 Levels as A Marker of Macrophage Activation in Polymyositis and Dermatomyosits: Associated with Macrophage Infiltration in Muscle Tissue
  1. Q. Peng,
  2. X. Shu,
  3. X. Lu,
  4. G. Wang
  1. Department of Rheumatology, China-Japan Friendship Hospita, Beijing, China


Background CD163 is a monocyte/macrophage-restricted transmembrane glycoprotein and shedding of membrane CD163 through a proteolytic process produces soluble CD163 molecule (sCD163). The concentration of sCD163 in plasma may be a marker of monocyte/macrophage activity and number[1]. sCD163 was found increased in several autoimmune diseases such as rheumatoid arthritis, scleroderma, systemic lupus erythematosus[2]. However, information about serum sCD163 expression and its clinical significance in polymyositis (PM) and dermatomyosits (DM) is unkonwn.

Objectives The aim of this study was to investigate the serum sCD163 levels and their relation to clinical manifestations, as well as their association with macrophage infiltration in muscle tissue.

Methods Serum sCD163 levels were detected in 21 PM, 61 DM patients and 25 healthy controls by using the ELISA method. Disease activity was graded using the Myositis Disease Activity Assessment Visual Analog Scale. Immunohistochemistry staining of macrophage infiltration in muscle tissue by anti-CD163 monoclonal antibody was conducted on muscle biopsy specimens from 17 DM patients and 13 PM patients. Statistical analysis was performed using SPSS V.16.0.

Results Serum sCD163 levels were significantly increased in the PM/DM patients compared to those in the healthy controls (P<0.001), and serum sCD163 levles of DM patients was statistically higher than that of PM patients (P<0.001). In particular, patients with interstitial lung disease (ILD) have statistically higher sCD163 levels than patients without ILD (P<0.05). We defined a cut-off value of sCD163 as the mean plus 2 SD of the control subjects, which was 807 ng/ml, and then patients with high sCD163 were found to have significantly higher serum IgG levels (P<0.05) and higer serum IgA levels (P<0.05). Interestingly, serum sCD163 levels reversely correlated with CD3+ T cell numbers in PBMC of PM/DM patients (r=-0.259, P<0.05). Cross-sectional assessment of 67 patients revealed a mild correlation between serum sCD163 levels and disease activities (r=0.309, P<0.01). Serum sCD163 levels significantly decreased after treatment (P<0.01), along with the decreasing disease activity scores (P<0.01). The results of immunohistochemistry staining of macrophage infiltration in muscle tissue of PM/DM patients showed that 13 out of 17 DM patients were positive for CD163 antibody immunoreactivity, and 5 out of 13 PM patients were tested as CD163+ macrophage positive. The patients with high serum sCD163 level showed a significant higher frequency of CD163+ macrophage infiltration than patients with low serum sCD163 levels (13/15 vs 5/15, χ2 value=8.889, P<0.01).

Conclusions Serum sCD163 may probably be a useful biomarker in the disease evaluation of PM/DM, and associated with CD163+ macrophage infiltration in muscle tissue. In the light of sCD163 as a marker of macrophage activity, our study highlight the role of macrophage played in the pathogenesis of PM/DM. Further understanding of sCD163 and macrophage function in PM/DM may help to define therapeutic targets for PM/DM.


  1. Møller HJ. Soluble CD163. Scand J Clin Lab Invest. 2012,72(1):1-13.

  2. Etzerodt A, Moestrup SK. CD163 and inflammation: biological, diagnostic, and therapeutic aspects. Antioxid Redox Signal. 2013,18(17):2352-63.

Disclosure of Interest None declared

DOI 10.1136/annrheumdis-2014-eular.2784

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