Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease of the airways caused mainly by cigarette smoke exposure. COPD progression is marked by exacerbations of the disease, often associated with infections. Recent data show the involvement in COPD pathophysiology of interleukin (IL)-17 and IL-22, two cytokines that are important in the control of lung inflammation and infection. During the initiation and progression of the disease, increased IL-17 secretion causes neutrophil recruitment, leading to chronic inflammation, airways obstruction and emphysema. In the established phase of COPD, a defective IL-22 response facilitates pathogen-associated infections and disease exacerbations. Altered production of these cytokines involves a complex network of immune cells and dysfunction of antigen-presenting cells. In this review, we describe current knowledge on the involvement of IL-17 and IL-22 in COPD pathophysiology at steady state and during exacerbations, and discuss implications for COPD management and future therapeutic approaches. Alteration of IL-17 and IL-22 production plays a key role in COPD physiopathology and development of exacerbations http://ow.ly/zKFj30elgdw

中文翻译：

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Th17 细胞因子：COPD 发病机制和恶化的新潜在治疗靶点


慢性阻塞性肺疾病（COPD）是一种主要由吸烟引起的气道慢性炎症性疾病。 COPD 进展的特点是疾病恶化，通常与感染有关。最近的数据显示白细胞介素 (IL)-17 和 IL-22 参与 COPD 病理生理学，这两种细胞因子对于控制肺部炎症和感染很重要。在疾病的发生和进展过程中，IL-17 分泌增加导致中性粒细胞募集，导致慢性炎症、气道阻塞和肺气肿。在 COPD 的既定阶段，IL-22 反应缺陷会促进病原体相关感染和疾病恶化。这些细胞因子产生的改变涉及复杂的免疫细胞网络和抗原呈递细胞的功能障碍。在这篇综述中，我们描述了目前关于 IL-17 和 IL-22 在稳定状态和恶化期间参与 COPD 病理生理学的知识，并讨论了对 COPD 管理和未来治疗方法的影响。 IL-17 和 IL-22 产生的改变在 COPD 病理生理学和恶化的发展中起着关键作用 http://ow.ly/zKFj30elgdw