title: Circulating levels of the chemokine CCL18 but not CXCL16 are elevated and correlate with disease activity in rheumatoid arthritis.
abstract: BACKGROUND
  Antigen-presenting cells (APC) and T cells are considered to play a significant role in the pathogenesis of rheumatoid arthritis (RA). CCL18 and CXCL16 are two chemokines that facilitate T cell attraction by APC, of which a role in the pathogenesis of RA has been suggested.
  
  
  OBJECTIVE
  To compare the circulating levels of CXCL16 and CCL18 in RA with controls and to investigate the relation of CXCL16 and CCL18 with RA disease activity and joint damage.
  
  
  METHODS
  Circulating CCL18 and CXCL16 levels were determined in 61 RA patients with a follow-up of 6 years and a group of 41 healthy controls with ELISA. Chemokine levels were correlated with demographic data, disease activity (DAS28) and joint damage (modified Sharp score). In addition, serum CCL18 and CXCL16 levels from a cohort of 44 RA patients treated with anti-TNF-alpha were correlated with disease activity.
  
  
  RESULTS
  CCL18 levels in serum were significantly elevated in RA patients compared with controls, while serum CXCL16 levels were not. In contrast to CXCL16, serum CCL18 was positively correlated with disease activity. Both CCL18 and CXCL16 levels decreased upon treatment with anti-TNF-alpha. Neither CCL18 nor CXCL16 correlated with joint damage and progression.
  
  
  CONCLUSIONS
  Here, we show, for the first time, that circulating CCL18 and not CXCL16 levels are elevated in RA patients as compared with controls and correlate with disease activity in RA. More knowledge regarding the regulation and function of both CCL18 and CXCL16 is essential to value their role in RA.
authors.affiliation: Department of Rheumatology, Radboud University Nijmegen Medical Centre, The Netherlands.
authors.forename: Antoine W T
authors.initials: AW
authors.lastname: van Lieshout
authors.forename: Jaap
authors.initials: J
authors.lastname: Fransen
authors.forename: Marcel
authors.initials: M
authors.lastname: Flendrie
authors.forename: Agnes M M
authors.initials: AM
authors.lastname: Eijsbouts
authors.forename: Frank H J
authors.initials: FH
authors.lastname: van den Hoogen
authors.forename: Piet L C M
authors.initials: PL
authors.lastname: van Riel
authors.forename: Timothy R D J
authors.initials: TR
authors.lastname: Radstake
mesh_terms: D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D018501:Antirheumatic Agents / Q000627:therapeutic use; D001172:Arthritis, Rheumatoid / Q000097:blood* / Q000188:drug therapy / Q000473:pathology; D015415:Biomarkers / Q000097:blood; D000075743:Chemokine CXCL16; D019742:Chemokines, CC / Q000097:blood*; D019743:Chemokines, CXC / Q000097:blood*; D005260:Female; D006801:Humans; D000069285:Infliximab; D007596:Joints / Q000473:pathology; D008297:Male; D008875:Middle Aged; D051116:Receptors, Scavenger / Q000097:blood*; D012720:Severity of Illness Index; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
chemical_list: D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D015415:Biomarkers; C111792:CCL18 protein, human; C423727:CXCL16 protein, human; D000075743:Chemokine CXCL16; D019742:Chemokines, CC; D019743:Chemokines, CXC; D051116:Receptors, Scavenger; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab