title: CD4(+) CD25(+) regulatory T cells ameliorate Behcet's disease-like symptoms in a mouse model.
abstract: OBJECTIVE
  Behcet's disease (BD) is a chronic, multisystemic inflammatory disorder with arthritic, gastrointestinal, mucocutaneous, ocular, vascular and central nervous system involvement. It is well known that CD4(+) CD25(+) T-regulatory (Treg) cells prevent harmful immune responses to self- and non-self-antigens. In the present study, the role of Treg cells in herpes simplex virus (HSV)-induced BD-like symptoms was investigated.
  
  
  METHODS
  HSV type 1 (F strain) inoculation of the earlobe of ICR mice has been shown to induce the development of BD-like symptoms. To determine whether the effect of Treg was associated with change in BD-like symptoms, CD4(+) CD25(+) T cells from the splenocytes of normal mice were adoptively transferred intravenously. Treg cells of splenocytes were significantly elevated following the transfer of 3 × 10(5) CD4(+) CD25(+) T cells to BD-like mice compared with the control group.
  
  
  RESULTS
  The transfer of CD4(+) CD25(+) T cells to BD mice improved the symptoms, and the serum protein levels of interleukin (IL)-10, IL-6 and IL-17 were significantly altered compared with the control groups. Intravenous injection of anti-CD25 antibody to BD mice reduced the frequency of CD4(+) CD25(+) T cells and increased the BD severity score. We confirmed the influence of CD4(+) CD25(+) T cells on BD-like mice.
  
  
  CONCLUSIONS
  These results show that up-regulation of the CD4(+) CD25(+) T cells in BD-like mice improves the inflammatory symptoms, while down-regulation of CD25(+) T cells is associated with deteriorated symptoms. Furthermore, these findings are correlated with changes in pro-inflammatory and anti-inflammatory cytokine levels.
authors.affiliation: Laboratory of Cell Biology, Ajou University Institute for Medical Sciences, Suwon, Republic of Korea.
authors.forename: Jua
authors.initials: J
authors.lastname: Shim
authors.forename: Eun-So
authors.initials: ES
authors.lastname: Lee
authors.forename: Sun
authors.initials: S
authors.lastname: Park
authors.forename: Dongsik
authors.initials: D
authors.lastname: Bang
authors.forename: Seonghyang
authors.initials: S
authors.lastname: Sohn
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D001528:Behcet Syndrome / Q000276:immunology* / Q000378:metabolism / Q000628:therapy* / Q000821:virology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D002478:Cells, Cultured; D004195:Disease Models, Animal; D051858:Forkhead Transcription Factors / Q000276:immunology / Q000378:metabolism; D018259:Herpesvirus 1, Human / Q000472:pathogenicity; D007371:Interferon-gamma / Q000097:blood; D016753:Interleukin-10 / Q000097:blood; D020381:Interleukin-17 / Q000097:blood; D053645:Interleukin-2 Receptor alpha Subunit / Q000276:immunology*; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D013154:Spleen / Q000166:cytology / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*; D016212:Transforming Growth Factor beta / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D015854:Up-Regulation
chemical_list: D051858:Forkhead Transcription Factors; C498833:Foxp3 protein, mouse; C508018:Il2ra protein, mouse; D020381:Interleukin-17; D053645:Interleukin-2 Receptor alpha Subunit; D015850:Interleukin-6; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D007371:Interferon-gamma