title: IL-22+ CD4+ T cells in patients with rheumatoid arthritis.
abstract: OBJECTIVE
  Interleukin (IL)-22 regulates the pathogenesis of autoimmune diseases. The role of IL-22(+) T-cells in the pathogenesis of rheumatoid arthritis (RA) is unclear. This study aimed at examining the levels of plasma IL-22 and the frequency of IL-22(+) CD4(+) T-cells in patients with RA.
  
  
  METHODS
  A total of 30 RA patients and 18 gender- and age-matched healthy controls were recruited. Their peripheral blood mononuclear cells were isolated and stimulated with phorbol 12-myristate 13-acetate (PMA) and ionomycin for 6 h. The frequency of IL-22(+) , interferon (IFN)-γ(+) and IL-17A(+) CD4(+) T-cells was characterized by flow cytometry. The levels of plasma IFN-γ, IL-17A and IL-22, serum C-reactive protein (CRP), rheumatoid factor (RF), anticyclic citrullinated peptide antibody (CCP) and erythrocyte sedimentation rate (ESR) were measured.
  
  
  RESULTS
  The frequency of IFNγ(-) IL-17A(-)IL-22(+), IFNγ(-)IL-17A(+)IL-22(+), and IFNγ(+) IL-17A(-)IL-22(+) T-cells in CD4(+) T-cells and the levels of plasma IFNγ, IL-17 and IL-22 in RA patients were significant higher than those in healthy controls. The percentages of IL-17A(+)IL-22(+)CD4(+) T-cells were correlated positively with the frequency of Th22 or Th17 cells in the RA patients. The percentages of IL-22(+)CD4(+) T-cells were correlated positively with the values of disease activity score (DAS28) in the RA patients. The percentages of Th22 cells were correlated positively with the levels of plasma IL-22 in the RA patients.
  
  
  CONCLUSIONS
  Our data suggest that IL-22(+)CD4(+) T-cells may contribute to the pathogenesis of RA and that therapeutic targeting of IL-22 may be valuable for the intervention of RA.
authors.affiliation: Department of Rheumatology, the First Hospital, Jilin University, Changchun, China.
authors.forename: Ling
authors.initials: L
authors.lastname: Zhao
authors.forename: Zhenyu
authors.initials: Z
authors.lastname: Jiang
authors.forename: Yanfang
authors.initials: Y
authors.lastname: Jiang
authors.forename: Ning
authors.initials: N
authors.lastname: Ma
authors.forename: Yandong
authors.initials: Y
authors.lastname: Zhang
authors.forename: Li
authors.initials: L
authors.lastname: Feng
authors.forename: Kai
authors.initials: K
authors.lastname: Wang
mesh_terms: D000328:Adult; D000368:Aged; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000175:diagnosis / Q000276:immunology*; D001323:Autoantibodies / Q000097:blood; D015415:Biomarkers / Q000097:blood; D001799:Blood Sedimentation; D002097:C-Reactive Protein / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology* / Q000378:metabolism; D016022:Case-Control Studies; D002478:Cells, Cultured; D002681:China; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D016130:Immunophenotyping / Q000379:methods; D007371:Interferon-gamma / Q000097:blood; D020381:Interleukin-17 / Q000097:blood; D007378:Interleukins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D010456:Peptides, Cyclic / Q000276:immunology; D012720:Severity of Illness Index; D058504:Th17 Cells / Q000276:immunology / Q000378:metabolism; D000097043:Interleukin-22
chemical_list: D001323:Autoantibodies; D015415:Biomarkers; D002097:C-Reactive Protein; D007371:Interferon-gamma; D020381:Interleukin-17; D007378:Interleukins; D010456:Peptides, Cyclic; D000097043:Interleukin-22; C573415:IFNG protein, human; C508717:IL17A protein, human; C487763:cyclic citrullinated peptide
keywords: IL-22; Th1; Th17; Th22; rheumatoid arthritis