Epithelial-Derived Cytokines in Asthma
Epithelial-Derived Cytokines in Asthma
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DOI：
10.1016/j.chest.2016.10.042
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发表时间：
2017-06-01
期刊：
影响因子：
9.6
通讯作者：
O'Byrne, Paul M.
中科院分区：
文献类型：
--
作者：
Mitchell, Patrick D.;O'Byrne, Paul M.
气道上皮细胞和吸入环境之间的相互作用对于理解哮喘的病理生物学至关重要。一些研究已经确定了气道上皮源性细胞因子IL-25、IL-33和胸腺基质淋巴细胞生成素（TSLP）在哮喘发病机制中的重要作用。这些细胞因子已被描述为上皮来源的alarmin，其在存在实际或感知损伤的情况下激活并增强免疫系统的先天和体液臂。三种上皮来源的alarmin中的每一种都与吸入性变应原诱导的气道反应的病理生物学有关。迄今为止，关于TSLP的最佳证据在于，结合TSLP并阻止其与其受体结合的人单克隆抗体解决了过敏性哮喘患者的气道炎症并减弱了过敏原诱导的气道反应。更好地了解上皮来源的alarmins所起的作用以及它们如何影响气道免疫反应，可能有助于开发用于哮喘治疗的新疗法。
The interaction between the airway epithelium and the inhaled environment is crucial to understanding the pathobiology of asthma. Several studies have identified an important role of airway epithelial-derived cytokines, IL-25, IL-33, and thymic stromal lymphopoietin (TSLP) in asthma pathogenesis. These cytokines have been described as epithelial-derived alarmins that activate and potentiate the innate and humoral arms of the immune system in the presence of actual or perceived damage. Each of the three epithelial-derived alarmins has been implicated in the pathobiology of inhaled allergen-induced airway responses. The best evidence to date exists for TSLP, in that a human monoclonal antibody, which binds TSLP and prevents its engagement with its receptor, resolves airway inflammation in patients with allergic asthma and attenuates allergen-induced airway responses. Better understanding the roles that the epithelial-derived alarmins play and how they influence airway immune response may allow the development of novel therapeutics for asthma treatment.