ABSTRACT

Introduction: Bronchial asthma (BA) is a chronic airways inflammatory disease. Based on the biological mechanisms that underline the disease, asthma has been classified as type 2 or non-type 2 phenotype.

Areas covered: An emerging role has been identified for group 2 innate lymphoid cells (ILC2s) able to produce the classical type 2 cytokines. The role of Th2 cells and IL-4 is crucial in the pathogenesis of allergic BA as supported by asthma models. IL-13, shares many biological functions with IL-4 such as induction of IgE synthesis and regulation of eosinophil trafficking. However, IL-13 does not induce Th2 cell differentiation. The Authors reviewed evidence on the new concept of type 2 inflammation and the cellular and molecular network behind this process. Literature data in the PubMed were analyzed for peer-reviewed articles published until September 2020.

Expert opinion: The current trend is to consider Th2- and ILC2-driven pathways as two separate pathogenic mechanisms, recent data underscore that adaptive Th2- and innate cell responses represent two integrated systems in the production of IL-4, IL-5, and IL-13 leading to the current ‘concept’ of type 2 inflammation. This review highlights the role of Th2 cells and ILC2 in the recent new concept of type 2 inflammation.

摘要

简介：支气管哮喘（BA）是一种慢性气道炎症性疾病。基于强调该疾病的生物学机制，哮喘已被归类为 2 型或非 2 型表型。

涵盖的领域： 已经确定了能够产生经典 2 型细胞因子的第 2 组先天淋巴细胞 (ILC2) 的新兴作用。正如哮喘模型所支持的那样，Th2 细胞和 IL-4 的作用在过敏性 BA 的发病机制中至关重要。IL-13 与 IL-4 具有许多生物学功能，例如诱导 IgE 合成和调节嗜酸性粒细胞运输。然而，IL-13 不诱导 Th2 细胞分化。作者回顾了关于 2 型炎症的新概念以及这一过程背后的细胞和分子网络的证据。对 PubMed 中的文献数据进行了分析，以获取 2020 年 9 月之前发表的同行评审文章。

专家意见：目前的趋势是将 Th2 和 ILC2 驱动的途径视为两个独立的致病机制，最近的数据强调适应性 Th2 和先天细胞反应代表了 IL-4、IL-5 和 IL-5 产生的两个集成系统。 IL-13 导致了当前 2 型炎症的“概念”。这篇综述强调了 Th2 细胞和 ILC2 在最近的 2 型炎症新概念中的作用。