title: Decoy receptor 3 suppresses B cell functions and has a negative correlation with disease activity in rheumatoid arthritis.
abstract: OBJECTIVE
  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%).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Medicine, National Yang-Ming University Hospital, Taiwan. meikankimo@yahoo.com.tw.
authors.forename: Ming-Han
authors.initials: MH
authors.lastname: Chen
authors.forename: Po-Chun
authors.initials: PC
authors.lastname: Liu
authors.forename: Chien-Wen
authors.initials: CW
authors.lastname: Chang
authors.forename: Yi-Ann
authors.initials: YA
authors.lastname: Chen
authors.forename: Ming-Huang
authors.initials: MH
authors.lastname: Chen
authors.forename: Chun-Yu
authors.initials: CY
authors.lastname: Liu
authors.forename: Chuen-Miin
authors.initials: CM
authors.lastname: Leu
authors.forename: Hsiao-Yi
authors.initials: HY
authors.lastname: Lin
mesh_terms: D000368:Aged; D001172:Arthritis, Rheumatoid / Q000175:diagnosis / Q000276:immunology / Q000378:metabolism*; D001402:B-Lymphocytes / Q000276:immunology / Q000378:metabolism*; D015415:Biomarkers / Q000378:metabolism; D016022:Case-Control Studies; D049109:Cell Proliferation; D002478:Cells, Cultured; D005260:Female; D006801:Humans; D008213:Lymphocyte Activation; D008297:Male; D008875:Middle Aged; D020370:Osteoarthritis, Knee / Q000175:diagnosis / Q000276:immunology / Q000378:metabolism; D053323:Receptors, Tumor Necrosis Factor, Member 6b / Q000378:metabolism*; D012720:Severity of Illness Index; D015398:Signal Transduction; D013582:Synovial Fluid / Q000276:immunology / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D015854:Up-Regulation
chemical_list: D015415:Biomarkers; D053323:Receptors, Tumor Necrosis Factor, Member 6b; C505911:TNFRSF6B protein, human; D014409:Tumor Necrosis Factor-alpha