Background. T-box expressed in T cells (TBET) and guanine adenine thymine adenine sequence-binding protein 3 (GATA3) play important roles in the differentiation of Th1 and Th2 subsets, which contributes to the progression of acute coronary syndrome (ACS). Objective. This study aimed to investigate the temporal change of TBET/GATA3 mRNA ratio in ACS. Methods. Thirty-three patients suspected of ACS with symptom onset within 24 hours were recruited. Blood samples were taken after arrival at the emergency department and at hourly intervals until the 6th hour. The mRNA expressions of TBET and GATA3 were quantified by a real-time RT-qPCR. Results. The TBET/GATA3 mRNA ratio was elevated dramatically in patients with acute myocardial infarction (AMI) and exhibited biphasic M-shaped release kinetics with two distinct peaks. The ratio was elevated 2 hours after symptom onset, dropped to the lowest level at 10 hours, and rose to the second peak at 14 hours. A similar biphasic M-shaped curve was observed in AMI patients with blood samples taken prior to any intervention. Conclusions. The TBET/GATA3 mRNA ratio was elevated in AMI patients throughout most of the first 20 hours after symptom onset. The biphasic M-shaped release kinetics was more likely to reflect pathophysiological changes rather than treatment effects. 1. Introduction On activation, T lymphocytes differentiate into T-helper (Th) 1 and Th2 subsets, and although the control of the Th1/Th2 imbalance is not fully elucidated, there is growing evidence to suggest that two transcription factors, T-box expressed in T cells (TBET) and guanine adenine thymine adenine sequence-binding protein 3 (GATA3), play important roles in such differentiation [1–4]. Th1 is essential in the process of plaque instability and plaque rupture, which in turn are common features in the pathogenesis of acute coronary syndrome (ACS) [5–7]. Upregulation of Th1 response has been demonstrated in the circulating lymphocytes of patients with ACS [6, 8]. In contrast, Th2 has rarely been shown in atherosclerotic lesions. Recent studies suggest that loss of Th1 and Th2 balance contributes to plaque rupture and the onset of ACS [6, 9]. Th1 and Th2 imbalances in the pathogenesis of ACS have been observed coherently from transcription to protein levels in both animal models and human subjects [8–13]. The relative expression of TBET and GATA3, resulting in a swing in the Th1/Th2 pendulum, has been implicated in several immunological diseases and may provide better prognostic and diagnostic information than downstream cytokines. In our recent
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