title: Impairment of Circulating CD4⁺CD25⁺GARP⁺ regulatory T cells in patients with acute coronary syndrome.
abstract: BACKGROUND
  Atherosclerosis (AS) is an inflammatory and immune disease. Regulatory T cells (Tregs) suppress the activation of T cells and have been shown to play a protective role during the pathogenesis of AS. However, specific markers for Tregs are lacking. Recently, glycoprotein A repetitions predominant (GARP) was discovered as a specific marker of activated Tregs, and we therefore utilized GARP as a specific surface marker for Tregs in the current study.
  
  
  METHODS
  To assess whether GARP(+) Tregs are downregulated in patients with acute coronary syndrome (ACS), we examined CD4(+)CD25(+)GARP(+) T cell frequencies as well as their associated cytokines and suppressive function. Additionally, we compared GARP expression to that of FOXP3, which may be more sensitive as a marker of activated Tregs in patients with ACS.
  
  
  RESULTS
  Patients with ACS demonstrated a significant decrease in circulating CD4(+)CD25(+)GARP(+) Tregs. Moreover, the suppressive function of Tregs and levels of related cytokines were also impaired in ACS patients compared to those with stable angina (SA) or normal coronary artery (NCA). Additionally, after TCR stimulation, peripheral blood mononuclear cells (PBMCs) from patients with ACS exhibited a decrease in CD4(+)CD25(+)GARP(+) Tregs.
  
  
  CONCLUSIONS
  These fnding indicate that circulating CD4(+)CD25(+)GARP(+) Tregs are impaired in patients withACS. Thus, targeting GARP may promote the protective function of Tregs in ACS.
authors.affiliation: The Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College, Huazhong, China.
authors.forename: Kai
authors.initials: K
authors.lastname: Meng
authors.forename: Wei
authors.initials: W
authors.lastname: Zhang
authors.forename: Yucheng
authors.initials: Y
authors.lastname: Zhong
authors.forename: Xiaobo
authors.initials: X
authors.lastname: Mao
authors.forename: Yingzhong
authors.initials: Y
authors.lastname: Lin
authors.forename: Ying
authors.initials: Y
authors.lastname: Huang
authors.forename: Mingjian
authors.initials: M
authors.lastname: Lang
authors.forename: Yudong
authors.initials: Y
authors.lastname: Peng
authors.forename: Zhengfeng
authors.initials: Z
authors.lastname: Zhu
authors.forename: Yuzhou
authors.initials: Y
authors.lastname: Liu
authors.forename: Xiaoqi
authors.initials: X
authors.lastname: Zhao
authors.forename: Kunwu
authors.initials: K
authors.lastname: Yu
authors.forename: Bangwei
authors.initials: B
authors.lastname: Wu
authors.forename: Qingwei
authors.initials: Q
authors.lastname: Ji
authors.forename: Qiutang
authors.initials: Q
authors.lastname: Zeng
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood / Q000276:immunology* / Q000473:pathology; D000368:Aged; D005260:Female; D051858:Forkhead Transcription Factors / Q000097:blood / Q000276:immunology; D005786:Gene Expression Regulation / Q000276:immunology; D006801:Humans; D053645:Interleukin-2 Receptor alpha Subunit / Q000097:blood / Q000276:immunology; D008297:Male; D008565:Membrane Proteins / Q000097:blood / Q000276:immunology*; D008875:Middle Aged; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000378:metabolism / Q000473:pathology
chemical_list: C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; C508017:IL2RA protein, human; D053645:Interleukin-2 Receptor alpha Subunit; C087215:LRRC32 protein, human; D008565:Membrane Proteins