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Interleukin-13 in Asthma and Other Eosinophilic Disorders

机译:IL-13在哮喘和其他嗜酸性粒细胞疾病中的作用

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Asthma is characterized by episodic, reversible airflow obstruction associated with variable levels of inflammation. Over the past several decades, there has been an increasing appreciation that the clinical presentation of asthma comprises a diverse set of underlying pathologies. Rather than being viewed as a single disease entity, asthma is now thought of as a clinical syndrome with the involvement of multiple pathological mechanisms. While it is appreciated that eosinophilia is present in only a subset of patients, it remains a key feature of asthma and other eosinophilic disorders such as atopic dermatitis, eosinophilic esophagitis, and chronic rhinosinusitis with nasal polyps. Eosinophils are bone marrow-derived leukocytes present in low numbers in health; however, during disease the type 2 cytokines [interleukins (IL)-4, -5, and -13] can induce rapid eosinophilopoiesis, prolonged eosinophil survival, and trafficking to the site of injury. In diseases such as allergic asthma there is an aberrant inflammatory response leading to eosinophilia, tissue damage, and airway pathology. IL-13 is a pleiotropic type 2 cytokine that has been shown to be integral in the pathogenesis of asthma and other eosinophilic disorders. IL-13 levels are elevated in animal models of eosinophilic inflammation and in the blood and tissue of patients diagnosed with eosinophilic disorders. IL-13 signaling elicits many pathogenic mechanisms including the promotion of eosinophil survival, activation, and trafficking. Data from preclinical models and clinical trials of IL-13 inhibitors in patients have revealed mechanistic insights into the role of this cytokine in driving eosinophilia. Promising results from clinical trials further support a key mechanistic role of IL-13 in asthma and other eosinophilic disorders. Here, we provide a perspective on the role of IL-13 in asthma and other eosinophilic disorders and describe ongoing clinical trials targeting this pathway in patients with significant unmet medical needs.
机译:哮喘的特征是发作性,可逆性气流阻塞,并伴有不同程度的炎症。在过去的几十年中,人们越来越认识到哮喘的临床表现包括多种潜在的病理学。如今,哮喘不再被视为单一疾病,而是被认为是一种涉及多种病理机制的临床综合征。尽管认识到嗜酸性粒细胞增多仅存在于一部分患者中,但它仍然是哮喘和其他嗜酸性粒细胞疾病的特有特征,例如特应性皮炎,嗜酸性粒细胞性食管炎和慢性鼻鼻窦炎伴鼻息肉。嗜酸性粒细胞是骨髓来源的白细胞,在健康中数量很少。但是,在疾病期间,2型细胞因子[白介素(IL)-4,-5和-13]可以诱导快速的嗜酸性粒细胞生成,延长的嗜酸性粒细胞存活以及运输到损伤部位。在诸如过敏性哮喘的疾病中,存在异常的炎症反应,导致嗜酸性粒细胞增多,组织损伤和气道病理。 IL-13是一种多效2型细胞因子,已被证明在哮喘和其他嗜酸性粒细胞疾病的发病机理中不可或缺。在嗜酸性粒细胞炎症的动物模型以及诊断为嗜酸性粒细胞疾病的患者的血液和组织中,IL-13水平升高。 IL-13信号传导引发许多致病机制,包括促进嗜酸性粒细胞的存活,活化和运输。来自患者中IL-13抑制剂的临床前模型和临床试验的数据揭示了对该细胞因子在驱动嗜酸性粒细胞增多中的作用的机理见解。临床试验的有希望的结果进一步支持了IL-13在哮喘和其他嗜酸性粒细胞疾病中的关键机制作用。在这里,我们提供了关于IL-13在哮喘和其他嗜酸性粒细胞疾病中的作用的观点,并描述了针对具有重大未满足医疗需求的患者针对该途径进行的正在进行的临床试验。

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