title: Imbalance of Th17/Treg cells in mice with chronic cigarette smoke exposure.
abstract: BACKGROUND
  Recent studies have revealed that autoimmune responses mediated by CD4(+) T cells may contribute to the development of chronic obstructive pulmonary disease (COPD). Meanwhile, imbalance of Th17/Treg has been reported to play a key role in the pathogenesis of autoimmune diseases. However, information on Th17/Treg balance in COPD is relatively limited.
  
  
  METHODS
  We established a mouse model of COPD induced by chronic cigarette smoke (CS) exposure. Th17 and Treg in lung tissue and peripheral blood were quantified by flow cytometry. The level of the specific transcription factors of both T cell subsets in lung tissue was determined by real-time PCR. The expressions of Th17- and Treg-related cytokines in serum and bronchoalveolar lavage fluid (BALF) were measured by enzyme-linked immunosorbent assay (ELISA).
  
  
  RESULTS
  We found that mice with chronic CS exposure showed significant increase in lung Th17 prevalence, retinoic acid orphan receptor (ROR)-γt mRNA and Th17-related cytokines (IL-17A, IL-6 and IL-23). Meanwhile, there was obvious decrease in Treg cell prevalence, Forkhead box (Fox) p3 mRNA and Treg-related cytokine IL-10, as compared to mice underwent sub-acute CS exposure and air-exposure. Similar tendency was also found for the Th17/Treg ratio in peripheral blood.
  
  
  CONCLUSIONS
  Our study thus reveals that the Th17/Treg imbalance exists in mice with chronic CS exposure, suggesting its potential role in the breakdown of immune self-tolerance in COPD. Further research on regulation of Th17/Treg balance may provide insights into the development of new therapeutic targets for this disease.
authors.affiliation: Department of Respiratory Diseases, Affiliated Yinzhou Hospital, College of Medicine, Ningbo University, Zhejiang Province 315040, PR China.
authors.forename: Huaying
authors.initials: H
authors.lastname: Wang
authors.forename: Weidong
authors.initials: W
authors.lastname: Peng
authors.forename: Yuesong
authors.initials: Y
authors.lastname: Weng
authors.forename: Huajuan
authors.initials: H
authors.lastname: Ying
authors.forename: Hequan
authors.initials: H
authors.lastname: Li
authors.forename: Dajing
authors.initials: D
authors.lastname: Xia
authors.forename: Wanjun
authors.initials: W
authors.lastname: Yu
mesh_terms: D000818:Animals; D051858:Forkhead Transcription Factors / Q000235:genetics / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects; D008168:Lung / Q000166:cytology / Q000187:drug effects / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000235:genetics / Q000378:metabolism; D029424:Pulmonary Disease, Chronic Obstructive / Q000139:chemically induced*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects* / Q000502:physiology; D058504:Th17 Cells / Q000187:drug effects* / Q000502:physiology; D013997:Time Factors; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*
chemical_list: D051858:Forkhead Transcription Factors; C498833:Foxp3 protein, mouse; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; D012333:RNA, Messenger; D014028:Tobacco Smoke Pollution