title: Reduced T-Cell Thymic Export Reflected by sj-TREC in Patients with Coronary Artery Disease.
abstract: OBJECTIVE
  Immunologic dysfunction was recently found to be one of the most important mechanisms underlying the initiation and development of atherosclerosis. Thymus involution can contribute to immune disturbance and disequilibrium of T-cell subsets. This study aimed to explore whether recent thymic emigration (RTE) is impaired in patients with coronary artery disease (CAD).
  
  
  METHODS
  Content of signal-joint T cell receptor excision circles (sj-TREC) in T lymphocytes, a molecular marker of RTE, was assessed among CAD patients and age-matched controls. Monochrome multiplex quantitative PCR method was used to assess the samples' telomere length in order to exclude the potential influence of T cell proliferation on the dilution of sj-TREC. Patients were grouped according to Gensini score (GS) (low, GS ＜18; intermediate, GS 18-41; high, GS ＞41). Ordinary logistic regression models were used to determine potential risk factors for CAD and GS tertiles.
  
  
  RESULTS
  Average copy numbers of sj-TREC per 10(6) T lymphocytes among patients with unstable angina, stable angina, and controls were 726±429, 1213±465, and 1795±838, respectively (P＜0.001). However, there was no significant difference in telomere length among groups. Moreover, the content of sj-TREC in the high GS group was most significantly reduced than the low GS group (P＜0.001). Multivariate logistic regression analysis revealed that lower sj-TREC was independently associated with the progression of CAD (OR=0.44, P＜0.001) and higher GS (OR=0.4, P＜0.001).
  
  
  CONCLUSIONS
  Impaired RTE could be partly responsible for CAD development. Mechanisms may be involved in the disturbance of T lymphocyte compartment and interruption of maintained immune tolerance resulting from thymus involution.
authors.affiliation: Department of Cardiology, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai, People's Republic of China.
authors.forename: Shuaibo
authors.initials: S
authors.lastname: Huang
authors.forename: Ru
authors.initials: R
authors.lastname: Ding
authors.forename: Yi
authors.initials: Y
authors.lastname: Lin
authors.forename: Zhiqing
authors.initials: Z
authors.lastname: He
authors.forename: Feng
authors.initials: F
authors.lastname: Wu
authors.forename: Xianliang
authors.initials: X
authors.lastname: Dai
authors.forename: Yihong
authors.initials: Y
authors.lastname: Chen
authors.forename: Yanping
authors.initials: Y
authors.lastname: Gui
authors.forename: Zhigang
authors.initials: Z
authors.lastname: Huang
authors.forename: Zonggui
authors.initials: Z
authors.lastname: Wu
authors.forename: Chun
authors.initials: C
authors.lastname: Liang
mesh_terms: D000367:Age Factors; D000368:Aged; D000369:Aged, 80 and over; D060050:Angina, Stable / Q000097:blood; D000789:Angina, Unstable / Q000097:blood; D049109:Cell Proliferation; D003324:Coronary Artery Disease / Q000276:immunology* / Q000503:physiopathology; D005260:Female; D006801:Humans; D007107:Immune System; D008213:Lymphocyte Activation; D018655:Lymphocyte Count; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D011446:Prospective Studies; D060888:Real-Time Polymerase Chain Reaction; D016176:T-Lymphocyte Subsets / Q000166:cytology*; D016615:Telomere / Q000648:ultrastructure