Cysteinyl Leukotrienes in Allergic Inflammation

IF 28.4 1区 医学 Q1 PATHOLOGY
Minkyu Lee, Joshua A. Boyce, Nora A. Barrett
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引用次数: 0

Abstract

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.
过敏性炎症中的胱氨酰白三烯
半胱氨酰白三烯(CysLTs)、LTC4、LTD4 和 LTE4 是花生四烯酸通过 5-脂氧合酶途径产生的强效脂质介质。这些介质通过三种不同的 G 蛋白偶联受体(GPCR)--CysLT1、CysLT2 和 OXGR1(又称 CysLT3 或 GPR99)--产生炎症和支气管收缩。虽然 CysLT 在过敏性炎症和哮喘的效应阶段所介导的功能已经确立了一段时间,但最近的研究表明,这些介质及其受体在诱导和扩大 2 型炎症方面发挥了新的作用。此外,体外研究和小鼠模型揭示了抑制或放大 CysLT 受体活化和 CysLT 受体功能的多种调节机制。本综述概述了 CysLT 的生物合成及其调控、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道疾病和 2 型炎症中的既有和新出现的作用。
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来源期刊
CiteScore
62.60
自引率
0.00%
发文量
40
期刊介绍: The Annual Review of Pathology: Mechanisms of Disease is a scholarly journal that has been published since 2006. Its primary focus is to provide a comprehensive overview of recent advancements in our knowledge of the causes and development of significant human diseases. The journal places particular emphasis on exploring the current and evolving concepts of disease pathogenesis, as well as the molecular genetic and morphological changes associated with various diseases. Additionally, the journal addresses the clinical significance of these findings. In order to increase accessibility and promote the broad dissemination of research, the current volume of the journal has transitioned from a gated subscription model to an open access format. This change has been made possible through the Annual Reviews' Subscribe to Open program, which allows all articles published in this volume to be freely accessible to readers. As part of this transition, all articles in the journal are published under a Creative Commons Attribution (CC BY) license, which encourages open sharing and use of the research.
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