title: Neutrophil CD64 expression in Behçet's disease.
abstract: OBJECTIVE
  Hyperfunction of neutrophils is a characteristic finding in Behçet's disease (BD). Microbial agents have been proposed as causative agents in the disease flares. Fc gamma receptor 1 (CD64) is not normally expressed by neutrophils of healthy individuals, but is upregulated by these cells in response to microbial wall components and proinflammatory cytokines. The degree of polymorphonuclear leukocyte (PMN) CD64 expression is different in autoimmune diseases and systemic infectious diseases. We investigated PMN CD64 expression in patients with BD.
  
  
  METHODS
  Thirty-seven patients with active BD (M/F: 18/19, mean age: 34.4 +/- 9.7 yrs), 35 patients with inactive BD (M/F: 11/24, mean age: 35.9 +/- 11.6 yrs), 27 patients with culture proven infections (M/F: 19/8, mean age: 54.4 +/- 15.2 yrs), 31 healthy controls (M/F: 14/17, mean age: 37.7 +/- 8.7 yrs), and 42 patients with active inflammatory disease (M/F: 13/29, mean age: 39.3 +/- 14.9 yrs) were enrolled in this study. Flow cytometry was used to assess the prevalence of CD64-bearing PMN in whole blood samples.
  
  
  RESULTS
  The prevalence of CD64-bearing PMN was significantly higher in patients with infectious disease (77.1 +/- 18.4), inflammatory disease (37.1 +/- 27.5), and active BD (48.9 +/- 22.5) than in healthy controls (9.5 +/- 7.8) or patients with inactive BD (12.9 +/- 9.5). CD64 expression was similar in controls and patients with inactive BD. In the infectious disease group, expression of CD64 was significantly higher than in the active BD and active inflammatory disease groups, while there was no significant difference between the groups of patients with active BD and inflammatory disorders.
  
  
  CONCLUSIONS
  Neutrophil CD64 expression increases during exacerbation of BD. This increase appears to be a non-specific inflammatory response and does not reflect PMN activation triggered by a living microorganism.
authors.affiliation: Department of Rheumatology, Hacettepe University School of Medicine, Ankara, Turkey.
authors.forename: Kemal
authors.initials: K
authors.lastname: Ureten
authors.forename: Ihsan
authors.initials: I
authors.lastname: Ertenli
authors.forename: M Akif
authors.initials: MA
authors.lastname: Oztürk
authors.forename: Sedat
authors.initials: S
authors.lastname: Kiraz
authors.forename: A Mesut
authors.initials: AM
authors.lastname: Onat
authors.forename: Murat
authors.initials: M
authors.lastname: Tuncer
authors.forename: Hamza
authors.initials: H
authors.lastname: Okur
authors.forename: Ali
authors.initials: A
authors.lastname: Akdogan
authors.forename: Sule
authors.initials: S
authors.lastname: Apras
authors.forename: Meral
authors.initials: M
authors.lastname: Calgüneri
mesh_terms: D000328:Adult; D001528:Behcet Syndrome / Q000453:epidemiology / Q000276:immunology* / Q000378:metabolism*; D015415:Biomarkers; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007239:Infections / Q000453:epidemiology / Q000276:immunology / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000276:immunology* / Q000378:metabolism*; D015995:Prevalence; D017452:Receptors, IgG / Q000378:metabolism*
chemical_list: D015415:Biomarkers; D017452:Receptors, IgG