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Respiratory viral infection, epithelial cytokines, and innate lymphoid cells in asthma exacerbations

机译:哮喘急性发作中的呼吸道病毒感染,上皮细胞因子和先天淋巴样细胞

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摘要

Exacerbations of asthma are most commonly triggered by viral infections, which amplify allergic inflammation. Cytokines released by virus-infected AECs may be important in driving this response. This review focuses on accumulating evidence in support of a role for epithelial cy-tokines, including IL-33, IL-25, and TSLP, as well as their targets, type 2 innate lymphoid cells (ILC2s), in the patho-genesis of virus-induced asthma exacerbations. Production and release of these cytokines lead to recruitment and activation of ILC2s, which secrete mediators, including IL-5 and IL-13, which augment allergic inflammation. However, little information is currently available about the induction of these responses by the respiratory viruses that are strongly associated with exacerbations of asthma, such as rhinoviruses. Further human studies, as well as improved animal experimental models, are needed to investigate appropriately the pathogenetic mechanisms in virus-induced exacerbations of asthma, including the role of ILCs.
机译:最常见的哮喘发作是由病毒感染引起的,病毒感染会加剧过敏性炎症。被病毒感染的AEC释放的细胞因子可能对推动这种反应很重要。这篇综述着重于积累证据支持上皮细胞因子包括IL-33,IL-25和TSLP以及它们的靶标2型先天淋巴样细胞(ILC2s)的发病机理。病毒引起的哮喘恶化。这些细胞因子的产生和释放导致ILC2的募集和激活,ILC2分泌包括IL-5和IL-13的介体,这些介体会增加过敏性炎症。但是,目前很少有信息与呼吸道疾病的发作有关,这些病毒与哮喘的发作密切相关,例如鼻病毒。需要进行进一步的人类研究,以及改进的动物实验模型,以适当研究病毒诱发的哮喘急性发作的致病机制,包括ILC的作用。

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