title: Imbalanced expression of dysfunctional regulatory T cells and T-helper cells relates to immunopathogenesis in polyarteritis nodosa.
abstract: OBJECTIVE
  We investigated the characteristics of circulating T-helper (Th) cells and CD4+regulatory T cells (Tregs) in polyarteritis nodosa (PAN).
  
  
  METHODS
  Peripheral blood samples were obtained from 14 patients with PAN. Nine patients having granulomatosis with polyangiitis (GPA) and 11 healthy individuals (HC) were enrolled as controls. Th cells and Tregs were analyzed by flow cytometry. Suppression assay of Tregs was simultaneously performed by evaluating the proliferation of conventional CD4+T cells cocultured with Tregs.
  
  
  RESULTS
  The frequencies of Th cells were significantly higher in PAN than in HC. In comparison with GPA, the expression of Th1 cells was higher but that of Th17 cells was lower. Additionally, significant increase in Tregs was observed in PAN, which was correlated with the expression of Th1 cells; however, defects in suppressive ability and CTLA-4 expression were observed. The Th1-cell frequency was significantly decreased after immunosuppressive therapy in PAN; however, there were no improvements in other phenotypes or in Treg function.
  
  
  CONCLUSIONS
  T-helper cell expansion and Treg dysfunction are thought to be associated with the pathogenesis of PAN. Th1 cells show a response to immunosuppressive therapy; however, the persistent immune abnormalities may interfere with complete recovery in patients with PAN.
authors.affiliation: a Department of Medicine (Neurology & Rheumatology) , Shinshu University School of Medicine , Matsumoto , Japan.
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Shimojima
authors.affiliation: a Department of Medicine (Neurology & Rheumatology) , Shinshu University School of Medicine , Matsumoto , Japan.
authors.forename: Wataru
authors.initials: W
authors.lastname: Ishii
authors.affiliation: a Department of Medicine (Neurology & Rheumatology) , Shinshu University School of Medicine , Matsumoto , Japan.
authors.forename: Dai
authors.initials: D
authors.lastname: Kishida
authors.affiliation: a Department of Medicine (Neurology & Rheumatology) , Shinshu University School of Medicine , Matsumoto , Japan.
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Fukushima
authors.affiliation: a Department of Medicine (Neurology & Rheumatology) , Shinshu University School of Medicine , Matsumoto , Japan.
authors.forename: Shu-Ichi
authors.initials: SI
authors.lastname: Ikeda
mesh_terms: D000328:Adult; D000368:Aged; D060908:CTLA-4 Antigen / Q000378:metabolism; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D010488:Polyarteritis Nodosa / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology / Q000378:metabolism / Q000473:pathology*
chemical_list: D060908:CTLA-4 Antigen; C556706:CTLA4 protein, human
keywords: CTLA-4; Polyarteritis nodosa; Regulatory T cells; T-helper cells