title: Increased frequencies of Th22 cells as well as Th17 cells in the peripheral blood of patients with ankylosing spondylitis and rheumatoid arthritis.
abstract: BACKGROUND
  T-helper (Th) 22 is involved in the pathogenesis of inflammatory diseases. The roles of Th22 cells in the pathophysiological of ankylosing spondylitis (AS) and rheumatoid arthritis (RA) remain unsettled. So we examined the frequencies of Th22 cells, Th17 cells and Th1 cells in peripheral blood (PB) from patients with AS and patients with RA compared with both healthy controls as well as patients with osteoarthritis.
  
  
  METHODS
  We studied 32 AS patients, 20 RA patients, 10 OA patients and 20 healthy controls. The expression of IL-22, IL-17 and IFN-γ were examined in AS, RA, OA patients and healthy controls by flow cytometry. Plasma IL-22 and IL-17 levels were examined by enzyme-linked immunosorbent assay.
  
  
  RESULTS
  Th22 cells, Th17 cells and interleukin-22 were significantly elevated in AS and RA patients compared with OA patients and healthy controls. Moreover, Th22 cells showed positive correlation with Th17 cells as well as interleukin-22 in AS and RA patients. However, positive correlation between IL-22 and Th17 cells was only found in AS patients not in RA patients. In addition, the percentages of both Th22 cells and Th17 cells correlated positively with disease activity only in RA patients not in AS patients.
  
  
  CONCLUSIONS
  The frequencies of both Th22 cells and Th17 cells were elevated in PB from patients with AS and patients with RA. These findings suggest that Th22 cells and Th17 cells may be implicated in the pathogenesis of AS and RA, and Th22 cells and Th17 cells may be reasonable cellular targets for therapeutic intervention.
authors.affiliation: Department of Orthopedics, Qilu Hospital, Shandong University, Jinan, China.
authors.forename: Lei
authors.initials: L
authors.lastname: Zhang
authors.forename: Yong-gang
authors.initials: YG
authors.lastname: Li
authors.forename: Yu-hua
authors.initials: YH
authors.lastname: Li
authors.forename: Lei
authors.initials: L
authors.lastname: Qi
authors.forename: Xin-guang
authors.initials: XG
authors.lastname: Liu
authors.forename: Cun-zhong
authors.initials: CZ
authors.lastname: Yuan
authors.forename: Nai-wen
authors.initials: NW
authors.lastname: Hu
authors.forename: Dao-xin
authors.initials: DX
authors.lastname: Ma
authors.forename: Zhen-feng
authors.initials: ZF
authors.lastname: Li
authors.forename: Qiang
authors.initials: Q
authors.lastname: Yang
authors.forename: Wei
authors.initials: W
authors.lastname: Li
authors.forename: Jian-min
authors.initials: JM
authors.lastname: Li
mesh_terms: D000328:Adult; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000276:immunology / Q000473:pathology*; D016022:Case-Control Studies; D002478:Cells, Cultured; D005260:Female; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism; D020381:Interleukin-17 / Q000097:blood; D007378:Interleukins / Q000097:blood; D008297:Male; D008875:Middle Aged; D013167:Spondylitis, Ankylosing / Q000097:blood / Q000276:immunology / Q000473:pathology*; D006377:T-Lymphocytes, Helper-Inducer / Q000378:metabolism / Q000473:pathology*; D018417:Th1 Cells / Q000378:metabolism / Q000473:pathology; D058504:Th17 Cells / Q000378:metabolism / Q000473:pathology*; D000097043:Interleukin-22
chemical_list: D007371:Interferon-gamma; D020381:Interleukin-17; D007378:Interleukins; D000097043:Interleukin-22