Eosinophil Granule Proteins

嗜酸性粒细胞颗粒蛋白质类
  • 文章类型: Journal Article
    嗜酸性粒细胞在机体的免疫反应中起着稳态作用。这些细胞参与对抗一些寄生虫,细菌,以及病毒感染和某些癌症,在包括哮喘在内的疾病中具有病理作用,慢性鼻-鼻窦炎伴鼻息肉,嗜酸性胃肠道疾病,和嗜酸性粒细胞增多综合征。传统上,嗜酸性粒细胞疾病的治疗是通过使用糖皮质激素进行非特异性嗜酸性粒细胞减弱。然而,几种针对嗜酸性粒细胞成熟因子的新型生物疗法,例如白细胞介素(IL)-5和IL-5受体或IL-4/IL-13最近已被批准用于临床使用。尽管生物疗法取得了成功,一些患有嗜酸性粒细胞炎性疾病的患者可能无法获得足够的症状控制,强调需要进一步调查患者特征的贡献,如合并症和其他过程,驱动正在进行的疾病活动。新的研究表明,嗜酸性粒细胞也参与几个稳态过程,包括新陈代谢,组织重塑和发育,神经元调节,上皮和微生物组调节,和免疫调节,表明这些细胞可能在健康人类的代谢调节和器官功能中起关键作用。因此,需要进一步研究嗜酸性粒细胞和嗜酸性粒细胞介导的过程在不同组织及其不同微环境中的稳态作用.这些工作可能为嗜酸性粒细胞不仅在疾病条件下而且在健康中的作用提供重要的见解。这篇叙述性综述综合了作者专业知识从PubMed检索的相关出版物,以提供对嗜酸性粒细胞在健康和疾病中的不同作用的新见解。特别强调嗜酸性粒细胞靶向治疗对当前和未来发展的影响。
    Eosinophils play a homeostatic role in the body\'s immune responses. These cells are involved in combating some parasitic, bacterial, and viral infections and certain cancers and have pathologic roles in diseases including asthma, chronic rhinosinusitis with nasal polyps, eosinophilic gastrointestinal disorders, and hypereosinophilic syndromes. Treatment of eosinophilic diseases has traditionally been through nonspecific eosinophil attenuation by use of glucocorticoids. However, several novel biologic therapies targeting eosinophil maturation factors, such as interleukin (IL)-5 and the IL-5 receptor or IL-4/IL-13, have recently been approved for clinical use. Despite the success of biologic therapies, some patients with eosinophilic inflammatory disease may not achieve adequate symptom control, underlining the need to further investigate the contribution of patient characteristics, such as comorbidities and other processes, in driving ongoing disease activity. New research has shown that eosinophils are also involved in several homeostatic processes, including metabolism, tissue remodeling and development, neuronal regulation, epithelial and microbiome regulation, and immunoregulation, indicating that these cells may play a crucial role in metabolic regulation and organ function in healthy humans. Consequently, further investigation is needed into the homeostatic roles of eosinophils and eosinophil-mediated processes across different tissues and their varied microenvironments. Such work may provide important insights into the role of eosinophils not only under disease conditions but also in health. This narrative review synthesizes relevant publications retrieved from PubMed informed by author expertise to provide new insights into the diverse roles of eosinophils in health and disease, with particular emphasis on the implications for current and future development of eosinophil-targeted therapies.
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  • 文章类型: Journal Article
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  • 文章类型: Journal Article
    The eosinophil has long been associated with diseases of acute hypersensitivity and with parasite infections, but its exact role in the pathogenesis of these conditions remains uncertain. Characterization of factors associated with migration of eosinophils into tissues has helped to elucidate eosinophil function. Eosinophil chemotactic factors associated with acute hypersensitivity reactions include the eosinophil chemotactic factors of anaphylaxis, histamine, and arachidonic acid metabolites, all of which are released from mast cells, and the lymphokine eosinophil stimulation promoter (ESP). Eosinophilotaxins associated with parasitic diseases include the lymphokine ESP and the low molecular weight factor ECF-G, both associated with schistosome infection in mice. In addition, in several parasite infections parasite-derived protein eosinophil chemotactic factors have been identified and characterized. The proteins associated with Ascaris, Anisakis, and Schistosoma infections appear to be distinct from one another. We have recently partially characterized a protein from Taenia taeniaeformis larvae which has marked chemotactic activity for eosinophils. In addition we have demonstrated eosinophil chemotactic activity associated with metabolism of arachidonic acid by T. taeniaeformis metacestodes. The results of studies in taeniasis and other parasite infections, therefore, indicate that parasite-derived factors may directly influence migration of eosinophils.
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