PDF(Pubmed)
Abstract：
Significant advancements have been achieved in understanding the roles of different immune cells, as well as cytokines and chemokines, in the pathogenesis of eosinophilic airway conditions. This review examines the pathogenesis of Chronic Rhinosinusitis with Nasal Polyps (CRSwNP), marked by complex immune dysregulation, with major contributions from type 2 inflammation and dysfunctional airway epithelium. The presence of eosinophils and the role of T-cell subsets, particularly an imbalance between Treg and Th17 cells, are crucial to the disease\'s pathogenesis. The review also investigates the pathogenesis of eosinophilic asthma, a unique asthma subtype. It is characterized by inflammation and high eosinophil levels, with eosinophils playing a pivotal role in triggering type 2 inflammation. The immune response involves Th2 cells, eosinophils, and IgE, among others, all activated by genetic and environmental factors. The intricate interplay among these elements, chemokines, and innate lymphoid cells results in airway inflammation and hyper-responsiveness, contributing to the pathogenesis of eosinophilic asthma. Another scope of this review is the pathogenesis of Eosinophilic Granulomatosis with Polyangiitis (EGPA); a complex inflammatory disease that commonly affects the respiratory tract and small to medium-sized blood vessels. It is characterized by elevated eosinophil levels in blood and tissues. The pathogenesis involves the activation of adaptive immune responses by antigens leading to T and B cell activation and eosinophil stimulation, which causes tissue and vessel damage. On the other hand, Allergic Bronchopulmonary Aspergillosis (ABPA) is a hypersensitive response that occurs when the airways become colonized by aspergillus fungus, with the pathogenesis involving activation of Th2 immune responses, production of IgE antibodies, and eosinophilic action leading to bronchial inflammation and subsequent lung damage. This analysis scrutinizes how an imbalanced immune system contributes to these eosinophilic diseases. The understanding derived from this assessment can steer researchers toward designing new potential therapeutic targets for efficient control of these disorders.
摘要：
在理解不同免疫细胞的作用方面取得了重大进展，以及细胞因子和趋化因子，在嗜酸性粒细胞气道疾病的发病机理中。这篇综述探讨了慢性鼻-鼻窦炎伴鼻息肉（CRSwNP）的发病机制，以复杂的免疫失调为标志，主要来自2型炎症和功能失调的气道上皮。嗜酸性粒细胞的存在和T细胞亚群的作用，特别是Treg和Th17细胞之间的不平衡，对疾病的发病机制至关重要。该综述还调查了嗜酸性粒细胞性哮喘的发病机理，一种独特的哮喘亚型.它的特点是炎症和高嗜酸性粒细胞水平，嗜酸性粒细胞在引发2型炎症中起关键作用。免疫反应涉及Th2细胞，嗜酸性粒细胞,和IgE,其中,都是由遗传和环境因素激活的。这些元素之间错综复杂的相互作用，趋化因子,和先天淋巴细胞导致气道炎症和高反应性，有助于嗜酸性粒细胞性哮喘的发病机制。本综述的另一个范围是嗜酸性肉芽肿性血管炎（EGPA）的发病机理；一种复杂的炎症性疾病，通常影响呼吸道和中小型血管。其特征在于血液和组织中嗜酸性粒细胞水平升高。发病机制涉及通过导致T和B细胞活化和嗜酸性粒细胞刺激的抗原激活适应性免疫应答。导致组织和血管损伤。另一方面,过敏性支气管肺曲霉病（ABPA）是一种过敏反应，当气道被曲霉菌定植时发生，发病机制涉及激活Th2免疫反应，IgE抗体的产生，和嗜酸性粒细胞的作用导致支气管炎症和随后的肺损伤。该分析仔细检查了不平衡的免疫系统如何导致这些嗜酸性粒细胞疾病。从这种评估中得出的理解可以引导研究人员设计新的潜在治疗靶标，以有效控制这些疾病。
