title: [The role of CD4+ CD25+ regulatory T cells in the pathogenesis of asthma in children].
abstract: OBJECTIVE
  To investigate the role of CD4(+)CD25(+) regulatory T cells (Tr cells) in the pathogenesis of asthma in children.
  
  
  METHODS
  Peripheral blood samples were collected from 20 pediatric patients with asthma, 10 male and 10 female, aged 7 (3-12), and 20 healthy children, 10 male and 10 female, aged 6.5 (2-11). Lymphocytes were isolated. Flow cytometry was used to examine the percentages of CD4(+)CD25(+) regulatory T cells, IL-10 secreting CD4(+)CD25(+) regulatory T cells (CD4(+)CD25(+)-IL-10), and transforming growth factor (TGF)-beta secreting CD4(+)CD25(+) regulatory T cells (CD4(+)CD25(+)-TGF-beta). RT-PCR and real-time PCR were used to detect the mRNA expression of suppressor of cytokine signal 1 (SOSC1) and Foxp3.
  
  
  RESULTS
  The percentages of CD4(+)CD25(+) regulatory T cells of the asthma children was 6.51% +/- 1.94%, significantly lower than that of the healthy children (11.96% +/- 2.30%, P < 0.01); the percentage of CD4(+)CD25(+)-IL-10 of the asthma children was 1.46% +/- 0.35%, significantly lower than that of the healthy children (5.65% +/- 1.70%, P < 0.01); and the percentage of CD4(+)CD25(+)-TGF-beta of the asthma children was 1.24% +/- 0.21%, significantly lower than that t of the healthy children (4.23% +/- 1.65%, P < 0.01). The Foxp3 mRNA expression of the asthma children was 0.12 +/- 0.05, significantly lower than that of the healthy children (1.71 +/- 0.58, P < 0.01); and the SOCS1 mRNA expression of the asthma children was 0.38 +/- 0.19, significantly lower than that of the healthy children (1.51 +/- 0.41, P < 0.01).
  
  
  CONCLUSIONS
  The decrease of CD4(+)CD25(+) regulatory T cells may be involved in the pathogenesis of asthma. The decreased mRNA expression of Foxp3 and SOCS1 may be associated with the aberrant development of CD4(+)CD25(+) regulatory T cells.
authors.affiliation: Shenzhen Institute of Pediatrics, Shenzhen Children's Hospital, Shenzhen 518026, China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Zu
authors.forename: Cheng-rong
authors.initials: CR
authors.lastname: Li
authors.forename: Yue-jie
authors.initials: YJ
authors.lastname: Zheng
authors.forename: Ji-kui
authors.initials: JK
authors.lastname: Deng
authors.forename: Xiao-ling
authors.initials: XL
authors.lastname: Fu
mesh_terms: D001249:Asthma / Q000097:blood / Q000276:immunology* / Q000503:physiopathology; D002648:Child; D002675:Child, Preschool; D005260:Female; D005434:Flow Cytometry; D051858:Forkhead Transcription Factors / Q000235:genetics; D006801:Humans; D016753:Interleukin-10 / Q000032:analysis; D053645:Interleukin-2 Receptor alpha Subunit / Q000032:analysis*; D008297:Male; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D000071222:Suppressor of Cytokine Signaling 1 Protein; D050826:Suppressor of Cytokine Signaling Proteins / Q000235:genetics; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000502:physiology; D016212:Transforming Growth Factor beta / Q000032:analysis
chemical_list: C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; D053645:Interleukin-2 Receptor alpha Subunit; D012333:RNA, Messenger; C108944:SOCS1 protein, human; D000071222:Suppressor of Cytokine Signaling 1 Protein; D050826:Suppressor of Cytokine Signaling Proteins; D016212:Transforming Growth Factor beta; D016753:Interleukin-10