The cysteinyl leukotrienes (CysLTs), LTC4, LTD4, and LTE4, are potent lipid mediators derived from arachidonic acid through the 5-lipoxygenase pathway. These mediators produce both inflammation and bronchoconstriction through three distinct G protein–coupled receptors (GPCRs)—CysLT1, CysLT2, and OXGR1 (also known as CysLT3 or GPR99). While CysLT-mediated functions in the effector phase of allergic inflammation and asthma have been established for some time, recent work has demonstrated novel roles for these mediators and their receptors in the induction and amplification of type 2 inflammation. Additionally, in vitro studies and murine models have uncovered diverse regulatory mechanisms that restrain or amplify CysLT receptor activation and CysLT receptor function. This review provides an overview of CysLT biosynthesis and its regulation, the molecular and functional pharmacology of CysLT receptors, and an overview of the established and emerging roles of CysLTs in asthma, aspirin-exacerbated respiratory disease, and type 2 inflammation.

中文翻译：

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半胱氨酰白三烯治疗过敏性炎症


半胱氨酰白三烯 （CysLTs）、LTC4、LTD4 和 LTE4 是通过 5-脂氧合酶途径从花生四烯酸衍生的有效脂质介质。这些介质通过三种不同的 G 蛋白偶联受体 （GPCR） —CysLT1、CysLT2 和 OXGR1（也称为 CysLT3 或 GPR99）产生炎症和支气管收缩。虽然 CysLT 介导的在过敏性炎症和哮喘效应期的功能已经建立有一段时间了，但最近的工作已经证明这些介质及其受体在 2 型炎症的诱导和放大中具有新的作用。此外，体外研究和小鼠模型揭示了抑制或扩增 CysLT 受体激活和 CysLT 受体功能的多种调节机制。本综述概述了 CysLT 的生物合成及其调节、CysLT 受体的分子和功能药理学，并概述了 CysLTs 在哮喘、阿司匹林加重的呼吸系统疾病和 2 型炎症中的既定和新兴作用。