title: Changes in expression of T-helper (Th) 1- and Th2-associated chemokine receptors on peripheral blood lymphocytes and plasma concentrations of their ligands, interferon-inducible protein-10 and thymus and activation-regulated chemokine, after antithyroid drug administration in hyperthyroid patients with Graves' disease.
abstract: OBJECTIVE
  Although Graves' disease is considered an autoantibody-mediated, T-helper 2 (Th2)-dominant disease, Th1-dominance may prevail in its initial phase. We longitudinally investigated Th1/Th2 balance in untreated hyperthyroid patients with Graves' disease after treatment of methimazole (MMI), an antithyroid drug.
  
  
  METHODS
  University clinic outpatients were studied prospectively.
  
  
  METHODS
  Subjects included 23 untreated hyperthyroid patients with Graves' disease and 17 age-matched control subjects.
  
  
  METHODS
  Before and after treatment, we measured Th1- and Th2-associated chemokine receptors (CXCR)3 and CCR4, on peripheral blood lymphocytes using flow cytometry, as well as plasma concentrations of their ligands, interferon-inducible protein (IP)-10 and thymus and activation-regulated chemokine (TARC).
  
  
  RESULTS
  The percentage of CXCR3-expressing cells among CD4+T lymphocytes and plasma IP-10 was significantly higher in hyperthyroid Graves' disease patients than in controls. At 12 and 24 weeks after initiation of MMI, percentage of CXCR3-expressing CD4+T lymphocytes had decreased significantly, while the percentage of CCR4-expressing CD4+T lymphocytes had increased significantly at 24 weeks. The CXCR3/CCR4 ratio had decreased significantly at 24 weeks. Plasma concentrations of IP-10 had decreased significantly at 12 and 24 weeks. Plasma concentrations of TARC also had decreased significantly at 24 weeks.
  
  
  CONCLUSIONS
  In hyperthyroid patients with Graves' disease in the active phase, Th1 cells rather than Th2 cells predominated among peripheral blood lymphocytes. After initiation of MMI, an ongoing transition from Th1 to Th2 dominance occurred.
authors.affiliation: Department of Internal Medicine, Koshigaya Hospital, Dokkyo Medical University, 2-1-50 Minami-Koshigaya, Koshigaya, Saitama 343-8555, Japan.
authors.forename: Yoshihisa
authors.initials: Y
authors.lastname: Inukai
authors.forename: Atsushi
authors.initials: A
authors.lastname: Momobayashi
authors.forename: Naoto
authors.initials: N
authors.lastname: Sugawara
authors.forename: Yoshimasa
authors.initials: Y
authors.lastname: Aso
mesh_terms: D000328:Adult; D013956:Antithyroid Agents / Q000008:administration & dosage*; D015415:Biomarkers / Q000378:metabolism; D054414:Chemokine CCL17; D054357:Chemokine CXCL10; D019742:Chemokines, CC / Q000378:metabolism; D019743:Chemokines, CXC / Q000097:blood*; D005260:Female; D005434:Flow Cytometry; D006111:Graves Disease / Q000188:drug therapy* / Q000276:immunology*; D006801:Humans; D008024:Ligands; D008297:Male; D008713:Methimazole / Q000008:administration & dosage*; D008875:Middle Aged; D011446:Prospective Studies; D054398:Receptors, CCR4; D054367:Receptors, CXCR3; D019707:Receptors, Chemokine / Q000378:metabolism; D018417:Th1 Cells / Q000187:drug effects / Q000378:metabolism*; D018418:Th2 Cells / Q000187:drug effects / Q000378:metabolism*; D013950:Thymus Gland / Q000166:cytology / Q000276:immunology
chemical_list: D013956:Antithyroid Agents; D015415:Biomarkers; C106230:CCL17 protein, human; C515354:CCR4 protein, human; C515187:CXCR3 protein, human; D054414:Chemokine CCL17; D054357:Chemokine CXCL10; D019742:Chemokines, CC; D019743:Chemokines, CXC; D008024:Ligands; D054398:Receptors, CCR4; D054367:Receptors, CXCR3; D019707:Receptors, Chemokine; D008713:Methimazole