Gunma Children's Medical Center, Department of Allergy and Immunology, Gunma Children's Medical Center, 779 Shimohakoda, Hokkitsu, Gunma 377-8577, Japan.
Expert Rev Clin Immunol. 2006 Jan;2(1):121-33. doi: 10.1586/1744666X.2.1.121.
Eosinophils are believed to play roles in the pathophysiology of allergic inflammation, such as bronchial asthma. However, recent studies on anti-interleukin-5 monoclonal antibody treatment of asthmatic patients raised the possibility that eosinophils may play only a limited role. More recent studies established that eosinophils are essentially involved in the development of airway remodeling. Moreover, it is theoretically conceivable that eosinophils are a cellular source of lipid mediators, such as cysteinyl leukotrienes or platelet-activating factor in asthma. Even in the absence of interleukin-5, it is likely that the 'T-helper Type 2 network', including a cascade of vascular cell adhesion molecule-1, intercellular cell adhesion molecule-1, CC chemokines, granulocyte-macrophage colony-stimulating factor, for example, can maintain sufficient eosinophilic infiltration and effector functions, such as superoxide anion generation and degranulation. Long-term studies, wherein tissue eosinophils are eliminated effectively will be required to establish the exact roles of these cells in asthma. Finally, the authors will demonstrate that eosinophils have the potential for not only playing detrimental roles but also beneficial ones.
嗜酸性粒细胞被认为在过敏性炎症的病理生理学中发挥作用,例如支气管哮喘。然而,最近关于抗白细胞介素-5 单克隆抗体治疗哮喘患者的研究提出了这样一种可能性,即嗜酸性粒细胞可能只发挥有限的作用。最近的研究还证实,嗜酸性粒细胞本质上参与了气道重塑的发展。此外,从理论上讲,可以想象嗜酸性粒细胞是哮喘中脂类介质(如半胱氨酰白三烯或血小板激活因子)的细胞来源。即使没有白细胞介素-5,包括血管细胞黏附分子-1、细胞间黏附分子-1、CC 趋化因子、粒细胞-巨噬细胞集落刺激因子等的“T 辅助细胞 2 型网络”,也可能维持足够的嗜酸性粒细胞浸润和效应功能,例如超氧阴离子生成和脱颗粒。需要进行长期研究,有效消除组织中的嗜酸性粒细胞,以确定这些细胞在哮喘中的确切作用。最后,作者将证明嗜酸性粒细胞不仅具有潜在的有害作用,也具有潜在的有益作用。
Expert Rev Clin Immunol. 2006-1
Auris Nasus Larynx. 2011-10
Nihon Kyobu Shikkan Gakkai Zasshi. 1996-12
Ann Ital Med Int. 1998
Eur Respir J Suppl. 1996-8
Allergy Asthma Clin Immunol. 2016-4-14
Front Pharmacol. 2013-4-17