Regulation of G-protein-coupled signaling pathways in allergic inflammation.
Regulation of G-protein-coupled signaling pathways in allergic inflammation.
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DOI：
10.1007/s12026-008-8050-0
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发表时间：
2009
影响因子：
4.4
通讯作者：
Druey, Kirk M.
中科院分区：
文献类型：
--
作者：
Druey, Kirk M.
关键词：
摘要过敏性疾病如哮喘是由免疫细胞如肥大细胞和淋巴细胞被其他无害的过敏原激活引起的。由这些细胞分泌的许多介质促进急性炎症，并且在许多情况下促进慢性组织重塑。这些化合物中的大多数通过激活G蛋白偶联受体（GPCR）对终末器官靶点如上皮和内皮细胞以及气道平滑肌发挥作用，GPCR是迄今为止最丰富的细胞表面受体类型。由于GPCR也是过敏治疗最常见的靶标，因此更好地了解其细胞内信号传导机制对于提高此类药物的疗效或开发新靶标至关重要。在这篇综述中，我们专注于一些新的调控元件，控制的持续时间和幅度的GPCR信号转导通路的免疫效应细胞和终末器官结构细胞受过敏性炎症。
Abstract Allergic diseases such as asthma are elicited by maladaptive activation of immune cells such as mast cells and lymphocytes by otherwise innocuous allergens. The numerous mediators secreted by such cells promote both acute inflammation and, in many instances, chronic tissue remodeling. Most of these compounds exert their effects on end-organ targets such as epithelial and endothelial cells and airway smooth muscle by activating G-protein-coupled receptors (GPCRs), which are by far the most abundant type of cell surface receptor. Since GPCRs are also the most common target of allergy therapeutics, a better understanding of their intracellular signaling mechanisms is vital to improve the efficacy of such drugs or to develop new targets. In this review, we focus on some of the new regulatory elements that control the duration and amplitude of GPCR signal transduction pathways in immune effector cells and end-organ structural cells affected by allergic inflammation.
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