首页> 美国卫生研究院文献>Journal of Leukocyte Biology >Respiratory viral infection epithelial cytokines and innate lymphoid cells in asthma exacerbations
【2h】

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

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

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 cytokines, including IL-33, IL-25, and TSLP, as well as their targets, type 2 innate lymphoid cells (ILC2s), in the pathogenesis 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,这种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。这篇综述着重于收集证据,以支持上皮细胞因子(包括IL-33,IL-25和TSLP)及其靶标2型先天淋巴样细胞(ILC2s)在病毒诱导的哮喘发病中的作用恶化。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在内的介质,这些介质会增加过敏性炎症。但是,目前很少有关于与哮喘发作加剧密切相关的呼吸道病毒(如鼻病毒)诱导这些反应的信息。需要进行进一步的人类研究,以及改进的动物实验模型,以适当地研究病毒诱发的哮喘急性发作的致病机制,包括ILC的作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号