title: Decreased levels of CCR3 in CD4+ lymphocytes of rheumatoid arthritis patients.
abstract: OBJECTIVE
  To evaluate the expression of CCR3 receptors as well as CCR3 agonists, including eotaxin-2 and RANTES, among patients suffering from rheumatoid arthritis and healthy controls, as a possible pathogenetic mechanism in inflammatory joint disease.
  
  
  METHODS
  Twenty-two patients and 13 healthy controls were recruited and clinically evaluated. CCR3 expression on CD4+ lymphocytes and mononuclear cells was evaluated by FACS analysis after staining with human CD4 APC (bioscience) and human CCR3 (CD193)PE. Levels of eotaxin-2 and RANTES were analysed by ELISA.
  
  
  RESULTS
  A significant decrease was observed in the level of CD4+ cells expressing the CCR3 receptor in serum of RA patients (0.96+/-0.5) as compared with healthy controls (1.48+/-0.6) (p<0.05). A significant decrease in serum eotaxin-2 levels was evident among RA patients suffering from active disease, defined by a DAS-28 score above 5.5, compared with RA patients with lower activity scores (2.1+/-1.6 vs. 7.0+/-5.1; p=0.01). A significant decrease was evident in the number of CCR3 expressing Monocytes among RA patients treated with steroids and anti TNF-a medications as compared with RA patients not receiving such treatment.
  
  
  CONCLUSIONS
  CCR3 is differentially expressed on inflammatory cells in RA, while eotaxin-2, a potent CCR3 agonist, is differentially expressed in active disease. Anti-inflammatory medications may down-regulate CCR3 expression in RA. The CCR3-CCR3 agonist pathway may thus have a pathogenic role in RA and may be a future target for novel treatment modalities.
authors.affiliation: Internal Medicine 6 and Institute of Rheumatology, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel. valeriea@tasmc.health.gov.il
authors.forename: V
authors.initials: V
authors.lastname: Aloush
authors.forename: J
authors.initials: J
authors.lastname: George
authors.forename: O
authors.initials: O
authors.lastname: Elkayam
authors.forename: I
authors.initials: I
authors.lastname: Wigler
authors.forename: S
authors.initials: S
authors.lastname: Oren
authors.forename: M
authors.initials: M
authors.lastname: Entin-Meer
authors.forename: S
authors.initials: S
authors.lastname: Maysel-Auslender
authors.forename: J N
authors.initials: JN
authors.lastname: Ablin
mesh_terms: D000328:Adult; D000368:Aged; D001172:Arthritis, Rheumatoid / Q000097:blood* / Q000188:drug therapy / Q000473:pathology; D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism* / Q000473:pathology; D016022:Case-Control Studies; D054423:Chemokine CCL24 / Q000097:blood; D018946:Chemokine CCL5 / Q000097:blood; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D054397:Receptors, CCR3 / Q000819:agonists / Q000097:blood*; D013256:Steroids / Q000627:therapeutic use; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
chemical_list: C515484:CCL24 protein, human; C515350:CCR3 protein, human; D054423:Chemokine CCL24; D018946:Chemokine CCL5; D054397:Receptors, CCR3; D013256:Steroids; D014409:Tumor Necrosis Factor-alpha