title: The Th17/Treg functional imbalance during atherogenesis in ApoE(-/-) mice.
abstract: OBJECTIVE
  Atherosclerosis is a chronic inflammatory disease regulated by T lymphocyte subsets. Recently, CD4(+) CD25(+) Foxp3(+) regulatory T (Treg) cells and Th17 cells have been described as two distinct subsets and have the opposite effects on autoimmunity. Clinical observation has revealed that the Th17/Treg imbalance exists in patients with acute coronary syndrome. We investigated whether the Th17/Treg functional imbalance existed during atherogenesis in ApoE(-/-) mice.
  
  
  RESULTS
  Th17/Treg functions at different levels including cell frequencies, related cytokine secretion and key transcription factors were investigated comparatively between ApoE(-/-) mice and their age-matched C57BL/6J mice. The results demonstrated that ApoE(-/-) mice revealed significantly increased secretion of Th17 related cytokines (IL-17 and IL-6) and expression of transcription factor (RORgammat) levels and obviously decreased number in Treg cells, secretion of Treg related cytokines (TGF-beta(1)) and expression of transcription factor (Foxp3) levels as compared with age-matched C57BL/6J mice. Th17 related mediators reached their maximum expression values at the early stage (8-16weeks of age) in ApoE(-/-) mice, and then followed by continuous depression of their expression levels. Meanwhile, the expression of Treg related mediators was much lower in ApoE(-/-) mice than in their age-matched wild-type littermates.
  
  
  CONCLUSIONS
  Th17/Treg functional imbalance exists during atherogenesis in ApoE(-/-) mice, suggesting a potential role of Th17/Treg imbalance in the formation and progression of atherosclerosis.
authors.affiliation: Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430022, China.
authors.forename: Jiang-jiao
authors.initials: JJ
authors.lastname: Xie
authors.forename: Jun
authors.initials: J
authors.lastname: Wang
authors.forename: Ting-ting
authors.initials: TT
authors.lastname: Tang
authors.forename: Jian
authors.initials: J
authors.lastname: Chen
authors.forename: Xing-li
authors.initials: XL
authors.lastname: Gao
authors.forename: Jing
authors.initials: J
authors.lastname: Yuan
authors.forename: Zi-hua
authors.initials: ZH
authors.lastname: Zhou
authors.forename: Meng-yang
authors.initials: MY
authors.lastname: Liao
authors.forename: Rui
authors.initials: R
authors.lastname: Yao
authors.forename: Xian
authors.initials: X
authors.lastname: Yu
authors.forename: Dan
authors.initials: D
authors.lastname: Wang
authors.forename: Yan
authors.initials: Y
authors.lastname: Cheng
authors.forename: Yu-hua
authors.initials: YH
authors.lastname: Liao
authors.forename: Xiang
authors.initials: X
authors.lastname: Cheng
mesh_terms: D000818:Animals; D001011:Aorta / Q000473:pathology; D001057:Apolipoproteins E / Q000235:genetics / Q000276:immunology*; D050197:Atherosclerosis / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D016207:Cytokines / Q000235:genetics / Q000276:immunology; D006801:Humans; D020381:Interleukin-17 / Q000235:genetics / Q000276:immunology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D016176:T-Lymphocyte Subsets / Q000166:cytology / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000166:cytology / Q000276:immunology*; D018417:Th1 Cells / Q000166:cytology / Q000276:immunology*
chemical_list: D001057:Apolipoproteins E; D016207:Cytokines; D020381:Interleukin-17