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Abstract：
Chronic rhinosinusitis with nasal polyps (CRSwNP) is predominantly a type 2 inflammatory disease associated with type 2 (T2) cell responses and epithelial barrier, mucociliary, and olfactory dysfunction. The inflammatory cytokines interleukin (IL)-4, IL-13, and IL-5 are key mediators driving and perpetuating type 2 inflammation. The inflammatory responses driven by these cytokines include the recruitment and activation of eosinophils, basophils, mast cells, goblet cells, M2 macrophages, and B cells. The activation of these immune cells results in a range of pathologic effects including immunoglobulin E production, an increase in the number of smooth muscle cells within the nasal mucosa and a reduction in their contractility, increased deposition of fibrinogen, mucus hyperproduction, and local edema. The cytokine-driven structural changes include nasal polyp formation and nasal epithelial tissue remodeling, which perpetuate barrier dysfunction. Type 2 inflammation may also alter the availability or function of olfactory sensory neurons contributing to loss of sense of smell. Targeting these key cytokine pathways has emerged as an effective approach for the treatment of type 2 inflammatory airway diseases, and a number of biologic agents are now available or in development for CRSwNP. In this review, we provide an overview of the inflammatory pathways involved in CRSwNP and describe how targeting key drivers of type 2 inflammation is an effective therapeutic option for patients.
摘要：
慢性鼻-鼻窦炎伴鼻息肉(CRSwNP)主要是与2型(T2)细胞反应和上皮屏障相关的2型炎症性疾病,粘膜纤毛，和嗅觉功能障碍。炎性细胞因子白细胞介素(IL)-4、IL-13和IL-5是驱动和维持2型炎症的关键介质。由这些细胞因子驱动的炎症反应包括嗜酸性粒细胞的募集和激活，嗜碱性粒细胞,肥大细胞,杯状细胞,M2巨噬细胞，B细胞。这些免疫细胞的激活导致一系列病理效应，包括免疫球蛋白E的产生，鼻粘膜内平滑肌细胞数量的增加和收缩性的降低，纤维蛋白原沉积增加，粘液过度产生,和局部水肿。细胞因子驱动的结构改变包括鼻息肉形成和鼻上皮组织重塑,从而延续屏障功能障碍。2型炎症也可能改变嗅觉感觉神经元的可用性或功能，导致嗅觉丧失。靶向这些关键的细胞因子途径已经成为治疗2型炎症性气道疾病的有效方法。和一些生物制剂现在可用或正在开发CRSwNP。在这次审查中,我们概述了与CRSwNP相关的炎症通路,并描述了针对2型炎症的关键驱动因素如何成为患者的有效治疗选择.
