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首页> 外文期刊>Current medicinal chemistry-Anti-inflammatory & anti-allergy agents.Anti-inflammatory & anti-allergy agents >Chemokines in allergic inflammation: human disease and animal models
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Chemokines in allergic inflammation: human disease and animal models

机译：在过敏性炎症趋化因子:人类疾病和动物模型

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The prevalence of allergic diseases has increased dramatically in the past 30 years. Inflammation, characterized by accumulation of eosinophils and T cells, and mast cell degranulation, plays a critical role in the pathogenesis of these diseases. Chemokines and their receptors are important in the control of leukocyte migration and are potential targets for therapeutic intervention. A large body of literature documents the increased presence of various chemokines and chemokine receptors in tissue samples collected from patients with allergic diseases, but the role of individual chemokines and chemokine receptors in the pathogenesis of allergic inflammation is often uncertain. Some progress has been made through the use of animal models of allergic disease, in which chemokines or chemokine receptors can be selective blocked with specific antibodies or genetically deleted This review discusses the immunopathology of allergic inflammation in asthma, allergic rhinitis and atopic dermatitis in human patients and in mouse models of allergic inflammation of the airway and skin. The role of chemokine receptors and their ligands is reviewed by comparing the expression of these molecules in human tissue samples and animal models, and by a discussion of the effect of selective manipulation of chemokines and chemokine receptors in animal models Human and mouse studies corroborate a critical role for CCR3 and its ligands in allergic inflammation, in particular in the infiltration of eosinophils, The role of chemokines and chemokine receptors in the accumulation of T cells and the migration and activation of mast cells is less clear and the delineation of their role may depend on the development and use of improved mouse models of chronic allergic inflammation.
机译：过敏性疾病的发病率增加了在过去的30年。以嗜酸性粒细胞和积累T细胞和肥大细胞脱颗粒,扮演了一个重要作用的发病机理疾病。重要的白细胞游走在控制和潜在的治疗目标干预。文件增加不同的存在趋化因子和趋化因子受体的组织样本收集的过敏患者疾病,但个别趋化因子的作用和趋化因子受体的发病机理过敏炎症通常是不确定的。进展通过使用动物过敏性疾病的模型,趋化因子可以选择性阻塞或趋化因子受体与特定的抗体和基因删除本文讨论的免疫病理反应过敏性哮喘炎症,过敏在人类患者鼻炎和过敏性皮炎和过敏性炎症的小鼠模型呼吸道和皮肤。综述了受体及其配体比较这些分子的表达人类组织样本和动物模型,通过一个讨论选择性的影响操纵的趋化因子和趋化因子受体在动物模型中人类和老鼠研究证实CCR3和至关重要的作用在过敏性炎症,其配体特定的嗜酸性粒细胞的浸润,趋化因子和趋化因子受体的作用T细胞的积累和迁移激活肥大细胞是不清楚的描述可能依赖于他们的角色改善小鼠模型的开发和使用慢性过敏性炎症。

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