A complex role for complement in allergic asthma.
A complex role for complement in allergic asthma.
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DOI：
10.1586/eci.09.84
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发表时间：
2010-03
影响因子：
4.4
通讯作者：
Köhl J
中科院分区：
文献类型：
--
作者：
Zhang X;Köhl J
过敏性哮喘是一种上呼吸道慢性炎症性疾病。人们普遍认为，适应不良的 Th2 免疫会促进过敏表型，但其潜在机制仍不清楚。这种疾病与补体的激活有关，补体是先天免疫系统中一种古老的危险感知成分。不同的实验性过敏性哮喘模型表明，C3 和 C5 的小补体片段、过敏毒素 C3a 和 C5a 不仅在过敏效应阶段促进促过敏效应功能，而且在过敏原致敏期间调节 Th2 免疫的发展。现有数据支持这样一个概念，即 C5a 在过敏原致敏过程中占主导地位，并防止适应不良的 Th2 免疫的发展。相比之下，C3a 和 C5a 似乎具有协同作用，并在效应阶段驱动过敏性炎症。在本文中，我们将回顾该领域的最新研究结果，以判断补体靶向治疗过敏性哮喘的益处。
Allergic asthma is a chronic inflammatory disease of the upper airway. It is well appreciated that maladaptive Th2 immunity promotes the allergic phenotype, the underlying mechanisms of which remain elusive. The disease is associated with activation of complement, an ancient danger-sensing component of the innate immune system. Different models of experimental allergic asthma suggest that the small complement fragments of C3 and C5, the anaphylatoxins C3a and C5a, not only promote proallergic effector functions during the allergic effector phase but regulate the development of Th2 immunity during allergen sensitization. The available data support a concept in which C5a is dominant during allergen sensitization and protects against the development of maladaptive Th2 immunity. By contrast, C3a and C5a appear to act synergistically and drive allergic inflammation during the effector phase. In this article, we will review the recent findings in the field to judge the benefit of complement targeting in allergic asthma.
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影响因子：
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