title: Analysis of T-cell receptor usage in myeloperoxidase--antineutrophil cytoplasmic antibody-associated renal vasculitis.
abstract: BACKGROUND
  Bacterial superantigens produced by Staphylococcus aureus may be associated with the onset of proteinase-3 antineutrophil cytoplasmic antibody (PR3-ANCA)-associated vasculitis, including Wegener's granulomatosis. We investigated T-cell subsets to assess the superantigens present in patients with myeloperoxidase-antineutrophil cytoplasmic antibody (MPO-ANCA)-associated vasculitis.
  
  
  METHODS
  Peripheral-blood mononuclear cells (PBMC) obtained from 40 normal controls and ten patients with MPO-ANCA-associated vasculitis were stained with fluorescence-labeled monoclonal antibodies against T-cell markers, including 17 variable regions of T-cell receptor beta-chains (TCR-Vbeta) and were then analyzed using flow cytometry.
  
  
  RESULTS
  Among PBMCs, the percentage of CD3(+) cells from patients with MPO-ANCA-associated vasculitis was significantly lower than that from normal controls, but there were no differences between the two groups in the percentage of CD19(+) cells or CD16(+) cells. Although there were no differences regarding the overall percentage of CD4(+) cells between the two groups, the percentage of CD4(+)CD45RO(+) cells in patients with MPO-ANCA-associated vasculitis was significantly higher than that in normal controls, and percentages of CD4(+)CD45RO(+)HLA-DR(+) and CD4(+)CD45RO(+)CD62L(low) cells in patients with MPO-ANCA-associated vasculitis were also significantly increased. There was no significant difference between the two groups in terms of the usage of the 17 different TCR-Vbeta regions.
  
  
  CONCLUSIONS
  There was no difference in bacterial superantigens between controls and MPO-ANCA-associated vasculitis patients because of the absence of specific usage of TCR-Vbeta regions. Given the elevated levels of memory T cells, conventional antigens rather than superantigens may be associated with the pathogenesis of MPO-ANCA-associated vasculitis.
authors.affiliation: Department of Nephrology, Tokyo Medical University Ibaraki Medical Center, 3-20-1 Chuo, Ami, Ibaraki, 300-0395, Japan, k-hira@tokyo-med.ac.jp.
authors.forename: Kouichi
authors.initials: K
authors.lastname: Hirayama
authors.forename: Takashi
authors.initials: T
authors.lastname: Ishizu
authors.forename: Homare
authors.initials: H
authors.lastname: Shimohata
authors.forename: Yasunori
authors.initials: Y
authors.lastname: Miyamoto
authors.forename: Tomoko
authors.initials: T
authors.lastname: Kakita
authors.forename: Miho
authors.initials: M
authors.lastname: Nagai
authors.forename: Yujiro
authors.initials: Y
authors.lastname: Ogawa
authors.forename: Shogo
authors.initials: S
authors.lastname: Fujita
authors.forename: Aki
authors.initials: A
authors.lastname: Hirayama
authors.forename: Kunihiro
authors.initials: K
authors.lastname: Yamagata
authors.forename: Masaki
authors.initials: M
authors.lastname: Kobayashi
authors.forename: Akio
authors.initials: A
authors.lastname: Koyama
mesh_terms: D000368:Aged; D019268:Antibodies, Antineutrophil Cytoplasmic / Q000276:immunology*; D017252:CD3 Complex / Q000032:analysis; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000276:immunology; D008297:Male; D008875:Middle Aged; D053146:Myeloblastin / Q000276:immunology*; D009195:Peroxidase / Q000276:immunology*; D011948:Receptors, Antigen, T-Cell / Q000276:immunology*; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D014657:Vasculitis / Q000276:immunology*
chemical_list: D019268:Antibodies, Antineutrophil Cytoplasmic; D017252:CD3 Complex; D011948:Receptors, Antigen, T-Cell; D009195:Peroxidase; D053146:Myeloblastin