Decoy receptor 3 suppresses B cell functions and has a negative correlation with disease activity in rheumatoid arthritis

Ming Han Chen, Po Chun Liu, Chien Wen Chang, Yi Ann Chen, Ming Huang Chen, Chun Yu Liu, Chuen Miin Leu, Hsiao Yi Lin*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

4 Scopus citations


Objectives: The decoy receptor 3 (DcR3) is a member of the tumour necrosis factor (TNF) receptor superfamily and may regulate inflammation. The aim of this study was to investigate the role of DcR3 in B cell functions and its correlation to disease activity in patients with rheumatoid arthritis (RA). Methods: The concentrations of DcR3 and TNF-α were measured by ELISA. B cell proliferation was assessed by quantification of 3H-thymidine uptake. Staphylococcus aureus Cowan (SAC) strain were used to stimulate B cell proliferation and TNF-α production. Results: Compared to the osteoarthritis (OA) patients, the RA group had higher synovial DcR3 levels (3273.6 ±1623.2 vs. 1594.8 ±1190.0 pg/ml, p =0.003), which were negatively correlated with the serum erythrocyte sedimentation rate and Disease Activity Score using 28 joint counts (DAS28) scores (r =-0.560, p =0.002; r =-0.579, p <0.001, respectively). Although the RA B cells have more active characteristics, B cell proliferation induced by SAC was successfully suppressed by recombinant DcR3.Fc fusion protein with an average inhibition of 44.8%. Moreover, DcR3.Fc fusion protein was found to suppress SAC-induced TNF-α production by B cells in 8 RA patients (average inhibition 47.0%). Conclusion: The results of our study indicated that the inhibition of B cell functions by DcR3 may partially explain the negative correlation between DcR3 level and disease activity in RA patients. Our findings imply that DcR3 may be used as a biomarker for disease activity and a potential therapeutic agent in the treatment of RA.

Original languageEnglish
Pages (from-to)715-723
Number of pages9
JournalClinical and Experimental Rheumatology
Issue number5
StatePublished - Oct 2014


  • B cell activation
  • Decoy receptor 3
  • Rheumatoid arthritis
  • Tumour necrosis factor-α


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