title: Human cartilage gp-39+,CD16+ monocytes in peripheral blood and synovium: correlation with joint destruction in rheumatoid arthritis.
abstract: OBJECTIVE
  To investigate the expression of human cartilage (HC) gp-39, a possible autoantigen in rheumatoid arthritis (RA), in peripheral blood and synovium, to characterize its cellular source, and to analyze correlations with clinical features.
  
  
  METHODS
  The expression of HC gp-39 in synovium and peripheral blood mononuclear cells (PBMC) was assessed by immunohistochemistry and flow cytometry. Synthesis and secretion were investigated by both reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay.
  
  
  RESULTS
  PBMC expressing HC gp-39 were increased in RA patients compared with spondylarthropathy patients (P = 0.0029) and with healthy control subjects (P = 0.0013). HC gp-39+ cells were also slightly overrepresented in RA synovium (P = 0.01). In both blood and synovium, HC gp-39+ cells were identified as CD14dim,CD16+ monocytes, a phenotype which can differentiate from classic CD14++ monocytes by maturation in vitro. HC gp-39 messenger RNA was detected in RA synovium and PBMC, and PBMC secreted HC gp-39 in vitro. The number of HC gp-39+ PBMC correlated with serum levels of C-reactive protein (r = 0.39, P = 0.003) and HC gp-39 (r = 0.52, P = 0.014). HC gp-39 expression in RA synovial lining correlated with joint destruction (r = 0.77, P < 0.001).
  
  
  CONCLUSIONS
  CD16+ monocytes, a cellular source of HC gp-39 in vivo, are overrepresented in both RA peripheral blood and synovial tissue. The presence of HC gp-39+ cells in RA synovium is correlated with the degree of joint destruction. These data support a role of these cells in the local autoimmune response that leads to chronic inflammation and joint destruction.
authors.affiliation: Department of Rheumatology, Ghent University Hospital, Belgium.
authors.forename: D
authors.initials: D
authors.lastname: Baeten
authors.forename: A M
authors.initials: AM
authors.lastname: Boots
authors.forename: P G
authors.initials: PG
authors.lastname: Steenbakkers
authors.forename: D
authors.initials: D
authors.lastname: Elewaut
authors.forename: E
authors.initials: E
authors.lastname: Bos
authors.forename: G F
authors.initials: GF
authors.lastname: Verheijden
authors.forename: G
authors.initials: G
authors.lastname: Berheijden
authors.forename: A M
authors.initials: AM
authors.lastname: Miltenburg
authors.forename: A W
authors.initials: AW
authors.lastname: Rijnders
authors.forename: E M
authors.initials: EM
authors.lastname: Veys
authors.forename: F
authors.initials: F
authors.lastname: De Keyser
mesh_terms: D054392:Adipokines; D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000097:blood / Q000378:metabolism*; D001172:Arthritis, Rheumatoid / Q000378:metabolism* / Q000473:pathology; D002358:Cartilage, Articular / Q000378:metabolism* / Q000473:pathology; D002454:Cell Differentiation; D002478:Cells, Cultured; D000071451:Chitinase-3-Like Protein 1; D005260:Female; D006023:Glycoproteins / Q000097:blood / Q000378:metabolism*; D006801:Humans; D037102:Lectins; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism* / Q000502:physiology; D010641:Phenotype; D013583:Synovial Membrane / Q000378:metabolism* / Q000473:pathology
chemical_list: D054392:Adipokines; D015703:Antigens, CD; C084533:CHI3L1 protein, human; D000071451:Chitinase-3-Like Protein 1; D006023:Glycoproteins; D037102:Lectins