IL-33 and Airway Inflammation.
IL-33 and Airway Inflammation.
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DOI：
10.4168/aair.2011.3.2.81
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发表时间：
2011-04
期刊：
影响因子：
--
通讯作者：
Saito H
中科院分区：
文献类型：
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作者：
Oboki K;Nakae S;Matsumoto K;Saito H
白细胞介素-33 （IL-33）是IL-1细胞因子家族的第11个成员，包括IL-1和IL-18。与IL-1β和IL-18不同，IL-33被认为是内皮细胞或上皮细胞损伤时释放的一种警报蛋白，可能不会通过激活炎性体来增强获得性免疫反应。ST2是一种IL-33受体成分，与Th1细胞、Th17细胞和中性粒细胞相比，ST2在t辅助型（Th） 2细胞、肥大细胞、嗜酸性粒细胞和嗜碱性粒细胞中优先表达。因此，IL-33通过增加过敏前细胞因子和趋化因子的表达，深刻地增强了过敏性炎症。事实上，最近的几项全基因组关联研究表明，IL-33及其受体基因被认为是哮喘的最易感基因。最近也有研究表明，IL-33在先天嗜酸性气道炎症中起关键作用，而不是获得性免疫反应，如IgE的产生。因此，IL-33为哮喘提供了一种独特的治疗方法，即改善先天性气道炎症。
Interleukin-33 (IL-33) is the 11th member of IL-1 cytokine family which includes IL-1 and IL-18. Unlike IL-1β and IL-18, IL-33 is suggested to function as an alarmin that is released upon endothelial or epithelial cell damage and may not enhance acquired immune responses through activation of inflammasome. ST2, a IL-33 receptor component, is preferentially expressed by T-helper type (Th) 2 cells, mast cells, eosinophils and basophils, compared to Th1 cells, Th17 cells and neutrophils. Thus, IL-33 profoundly enhances allergic inflammation through increased expression of proallergic cytokines and chemokines. Indeed, IL-33 and its receptor genes are recognized as the most susceptible genes for asthma by several recent genomewide association studies. It has also recently been shown that IL-33 plays a crucial role in innate eosinophilic airway inflammation rather than acquired immune responses such as IgE production. As such, IL-33 provides a unique therapeutic way for asthma, i.e., ameliorating innate airway inflammation.