title: Disturbed B cell homeostasis in newly diagnosed giant cell arteritis and polymyalgia rheumatica.
abstract: OBJECTIVE
  Several lines of evidence indicate that B cells may be involved in the immunopathology of giant cell arteritis (GCA) and polymyalgia rheumatica (PMR). This study was undertaken to examine the distribution of defined B cell subsets, including effector B (Beff) cells and regulatory B (Breg) cells, in patients with GCA and patients with PMR before and after corticosteroid treatment.
  
  
  METHODS
  Circulating B cells were analyzed in 34 newly diagnosed, untreated patients with GCA or PMR, and in 44 followup samples from patients with GCA or PMR who received corticosteroids for 2 weeks or 3 months. For comparison, 40 age-matched healthy controls and 11 rheumatoid arthritis (RA) patients were included. Serum BAFF levels were determined, and temporal arteries were studied by immunohistochemistry.
  
  
  RESULTS
  Patients newly diagnosed as having GCA or PMR, but not patients with RA, had decreased numbers of circulating B cells compared to healthy controls. B cell numbers recovered rapidly in treated patients with GCA and PMR in remission. This recovery was not achieved by compensatory hyperproliferation or enhanced bone marrow production. B cell numbers inversely correlated with erythrocyte sedimentation rates, C-reactive protein levels, and serum BAFF levels. Tumor necrosis factor α-positive Beff cells, but not interleukin-10 (IL-10)-positive Breg cells, were decreased in patients newly diagnosed as having GCA or PMR. Following treatment, circulating numbers of Beff cells normalized. The returning Beff cells demonstrated an enhanced capacity to produce IL-6. Few B cells were found in temporal artery biopsy specimens from GCA patients.
  
  
  CONCLUSIONS
  We show for the first time that the distribution of B cells is highly disturbed in GCA and PMR and that B cells likely contribute to the enhanced IL-6 response in both diseases.
authors.affiliation: University of Groningen and University Medical Center Groningen, Groningen, The Netherlands.
authors.forename: Kornelis S M
authors.initials: KS
authors.lastname: van der Geest
authors.forename: Wayel H
authors.initials: WH
authors.lastname: Abdulahad
authors.forename: Paulina
authors.initials: P
authors.lastname: Chalan
authors.forename: Abraham
authors.initials: A
authors.lastname: Rutgers
authors.forename: Gerda
authors.initials: G
authors.lastname: Horst
authors.forename: Minke G
authors.initials: MG
authors.lastname: Huitema
authors.forename: Mirjam P
authors.initials: MP
authors.lastname: Roffel
authors.forename: Caroline
authors.initials: C
authors.lastname: Roozendaal
authors.forename: Philip M
authors.initials: PM
authors.lastname: Kluin
authors.forename: Nicolaas A
authors.initials: NA
authors.lastname: Bos
authors.forename: Annemieke M H
authors.initials: AM
authors.lastname: Boots
authors.forename: Elisabeth
authors.initials: E
authors.lastname: Brouwer
mesh_terms: D000305:Adrenal Cortex Hormones / Q000627:therapeutic use; D000368:Aged; D001172:Arthritis, Rheumatoid / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism; D001402:B-Lymphocytes / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D060151:B-Lymphocytes, Regulatory / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D002454:Cell Differentiation / Q000276:immunology; D005260:Female; D005500:Follow-Up Studies; D013700:Giant Cell Arteritis / Q000188:drug therapy / Q000276:immunology* / Q000378:metabolism; D006706:Homeostasis / Q000276:immunology*; D006801:Humans; D015850:Interleukin-6 / Q000276:immunology / Q000378:metabolism; D016131:Lymphocyte Subsets / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D008297:Male; D011111:Polymyalgia Rheumatica / Q000188:drug therapy / Q000276:immunology* / Q000378:metabolism; D011446:Prospective Studies
chemical_list: D000305:Adrenal Cortex Hormones; C508600:IL6 protein, human; D015850:Interleukin-6