白介素33与支气管哮喘

Interleukin-33 and bronchial asthma

白介素33(IL-33)是2005年被发现的一个新的白介素家族成员。1989年ST2首先被Tominaga[1]鉴定为IL-1受体超家族的一个成员。后来Baekkevold等从高壁内皮细胞中分离得到IL-33分子[2],而且该分子定位于高壁内皮细胞的核内,故最初被称为"高壁内皮细胞来源的核因子"。直到2005年Schmitz等[3]发现高壁内皮细胞来源的核因子是ST2的特异性配体,并重新命名为IL-33。从那以后人们对IL-33的生物学特征有了更深入的了解。IL-33与ST2结合,诱导Th2细胞因子的产生,从而参与支气管哮喘等Th2相关疾病。本文就IL-33的分子结构、表达、生物学活性及其目前在支气管哮喘发病机制中的作用综述如下。

In 2005,interleukin-33 （IL 33） was reported as a newly described member of the IL-1 cytokine superfamily. In 1989, ST2 was first identified as a member of the IL 1 cytokine superfamily. After that, Baekkevold reported a nuclear factor present in endothelial cells of high endothelial venules （NF-HEV）, hence initially called NF-HEV. In 2005, Schmitz et al established that NF-HEV was the ligand for ST2, and renamed NF-HEV as IL-33. Since the year 2005, our understanding of the biology of IL-33 has advanced considerably. Along with Th2 activation, IL-33 strongly induces Th2 cytokine production and can promote the pathogenesis of Th2-related disease such as bronchial asthma. This review focuses on the molecular structure, expression, biology and contribution of IL-33 to the pathophysiology of bronchial asthma.