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AB0036 Soluble CD83 Plasma Levels Are Associated with Disease Activity and Course of Disease in Early Rheumatoid Arthritis
  1. A.-M. Kristensen1,
  2. M.L. Hetland2,
  3. K. Hørslev-Petersen3,
  4. P. Junker4,5,6,
  5. M. Østergaard2,
  6. K. Stengaard-Pedersen7,8,
  7. P. Höllsberg1,
  8. M. Hvid1,8,
  9. B. Deleuran1,7,8
  1. 1Department of Biomedicine, Aarhus University, Aarhus
  2. 2Copenhagen Center for Arthritis Research, Center for Rheumatology and Spine Diseases, Rigshospitalet, Glostrup
  3. 3King Christian 10th Hospital for Rheumatic Diseases, University of Southern Denmark
  4. 4Department of Rheumatology
  5. 5Department of Clinical Biochemistry and Pharmacology, Odense University Hospital
  6. 6Institute of Molecular Medicine, University of Southern Denmark, Odense
  7. 7Department of Rheumatology, Aarhus University Hospital
  8. 8Department of Clinical Medicine, Aarhus University, Aarhus, Denmark


Background The immune modulatory dendritic cell (DC) marker CD83 has previously been associated with autoimmune diseases.1,2 Levels of soluble CD83 (sCD83) are elevated in RA synovial fluid3, however the relation to clinical outcome of RA remains unknown. We hypothesize that CD83 plays a central role in the inflammatory process and disease development in RA.

Objectives To investigate the potential association of sCD83 with disease activity measures, treatment response and auto-antibody status in patients with early RA (eRA).

Methods Plasma samples from eRA (n=88) randomized to conventional DMARD treatment with or without 12 months of additional adalimumab therapy (MTX+ADA and MTX+PLA, respectively) were randomly selected from the OPERA cohort.4 A commercial sandwich ELISA was used to quantify plasma levels of sCD83 in patients and in age- and gender-matched healthy volunteers (HV, n=43). Spearman's rank correlation coefficient between soluble CD83 plasma levels and measures of disease activity (tender joint count (TJC28,40), swollen joint count (SJC28,40), DAS28 and CRP), treatment response (ACR20,50,70,90) and auto-antibody status (IgM-RF and ACPA) was calculated. All results are expressed as median with interquartile range and compared by non-parametric statistics.

Results At baseline, sCD83 in eRA was significantly higher than in HV plasma (168.5pg/ml (136.1pg/ml-203.5pg/ml) and 136.1pg/ml (116.9pg/ml-149.4pg/ml), respectively), p<0.0001. At 12 months follow-up sCD83 had decreased by approximately 10% (167.2 vs 151.2pg/ml, p=0006) in the MTX+PLA group while it remained unchanged in the MTX+ADA arm, (p=0.3).

In MTX+ADA (n=43) group baseline sCD83 levels correlated with ACR50 at 6 and 24 months (ρ= -0.33, p=0.04 and ρ= -0.34, p=0.03, respectively) and ACR90 at 24 months (ρ= -0.37, p=0.02). In the MTX+PLA (n=45) group baseline sCD83 levels were found to correlate with TJC28 at 12 and 24 months (ρ= -0.30, p=0.05 and ρ= -0.43, p=0.003, respectively) and TJC40 at 24 months (ρ= -0.32, p=0.04). sCD83 showed no association with IgM-RF and ACPA positivity.

Conclusions This study demonstrated that sCD83 levels were significantly elevated in eRA compared with HV. With additional adalimumab treatment, high sCD83 levels at baseline were sustained over time. A high sCD83 level at baseline was associated with changes in prospective disease activity parameters in both treatment groups, which points to a possible predictive value of sCD83 in eRA.

  1. Eckhardt J. et al. Mucosal immunol. Jul 2014;7(4):1006–1018.

  2. Starke C. et al. Immunobiology. Nov 2013;218(11):1411–1415.

  3. Hock BD. et al. Tissue antigens. Jan 2006;67(1):57–60.

  4. Horslev-Petersen K. et al. Ann Rheum Dis. Apr 2014;73(4):654–661.

Disclosure of Interest None declared

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