title: RANTES and monocyte chemoattractant protein 1 as sensitive markers of disease activity in patients with juvenile rheumatoid arthritis: a six-year longitudinal study.
abstract: OBJECTIVE
  To longitudinally investigate serum and synovial fluid (SF) levels of RANTES and monocyte chemoattractant protein 1 (MCP-1) as well as in vitro migration of mononuclear cells toward SF in patients with juvenile rheumatoid arthritis (JRA).
  
  
  METHODS
  Serum and SF levels of RANTES and MCP-1 were determined by enzyme-linked immunosorbent assay. Chemotaxis was performed using the modified Boyden chamber method.
  
  
  RESULTS
  Serum RANTES levels were significantly increased in all onset types of JRA, with the highest levels present in systemic-onset JRA. Serum MCP-1 levels were significantly elevated in patients with systemic-onset JRA and were associated with current systemic features. Although serum levels of RANTES and MCP-1 decreased significantly after treatment, RANTES and MCP-1 levels during disease remission were still significantly higher in JRA patients than in controls. A relationship was found between serum RANTES levels during remission and the duration of clinical remission, with low levels being associated with prolonged clinical remission and high levels with shorter clinical remission. Serum RANTES levels correlated with C-reactive protein concentrations, hemoglobin values, white blood cell (WBC) counts, and platelet counts, whereas serum MCP-1 levels correlated with WBC counts and serum ferritin levels. Levels of RANTES and MCP-1 in SF were elevated as compared with levels in serum. SF chemotactic activity for mononuclear leukocytes was significantly inhibited by either anti-RANTES or anti-MCP-1 antibody.
  
  
  CONCLUSIONS
  RANTES is a key molecule in the pathogenesis of all onset groups of JRA, whereas MCP-1 is particularly important in systemic-onset JRA. Serum levels of these CC chemokines represent more highly sensitive markers of disease activity than conventional markers of inflammation.
authors.affiliation: Chang Gung Children's Hospital and Chang Gung University, Taoyuan, Taiwan.
authors.forename: Tsung-Chieh
authors.initials: TC
authors.lastname: Yao
authors.forename: Ming-Ling
authors.initials: ML
authors.lastname: Kuo
authors.forename: Lai-Chu
authors.initials: LC
authors.lastname: See
authors.forename: Liang-Shiou
authors.initials: LS
authors.lastname: Ou
authors.forename: Wen-I
authors.initials: WI
authors.lastname: Lee
authors.forename: Chin-Kan
authors.initials: CK
authors.lastname: Chan
authors.forename: Jing-Long
authors.initials: JL
authors.lastname: Huang
mesh_terms: D000293:Adolescent; D001171:Arthritis, Juvenile / Q000175:diagnosis* / Q000378:metabolism*; D002465:Cell Movement; D018932:Chemokine CCL2 / Q000032:analysis*; D018946:Chemokine CCL5 / Q000032:analysis*; D002633:Chemotaxis / Q000276:immunology; D002648:Child; D002675:Child, Preschool; D005260:Female; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000276:immunology; D008137:Longitudinal Studies; D008297:Male; D013582:Synovial Fluid / Q000737:chemistry
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; D018946:Chemokine CCL5