近年来的研究已经报道证实了白细胞介素-33(IL-33)及其受体ST2可以保护心衰病人因机械应力过度牵拉所导致的心肌细胞肥大、心肌纤维化的发生以及可溶性ST2受体可作为潜在的心脏机械超负荷生物标志物。而对IL-33与受体ST2在动脉粥样硬化过程中发挥的作用少有涉及。本文主要探讨的是IL-33和ST2对抑制Th1/Th2漂移从而影响到动脉粥样硬化的进展以及血浆中可溶性ST2受体蛋白升高的意义。

Recent study has reported that interleukin-33(IL-33) and its receptor ST2 could prevent cardiomyocyte hypertrophy and exaggerated interstitial fibrosis which is because of the over harmful biomechanical force in patients with heart failure and soluble ST2 receptors is the potential biomarker of cardiac biomechanical overload. But few studies mentioned the sort of IL-33/ST2 complex plays a role in atherosclerosis. The purpose of this article is to explore the IL-33 and ST2 could reduce a Th1/Th2 shift. Consequently, it may improve the development of atherosclerosis and significance of soluble ST2 receptor increased in plasma.