重新探讨 MRGPRX2 在神经肌肉阻断药物过敏反应中的作用。
Revisiting the role of MRGPRX2 on hypersensitivity reactions to neuromuscular blocking drugs.
机构信息
Department of Basic and Translational Sciences, University of Pennsylvania, School of Dental Medicine, 240 South 40th Street, Philadelphia, PA 19104, USA.
出版信息
Curr Opin Immunol. 2021 Oct;72:65-71. doi: 10.1016/j.coi.2021.03.011. Epub 2021 Apr 12.
Abstract
Anaphylaxis is caused by a variety of triggers including Food and Drug Administration (FDA)-approved antibiotics, contrast media and neuromuscular blocking drugs (NMBDs). Traditionally, drug-induced anaphylaxis was thought to result mainly from IgE-mediated histamine release from mast cells. Recently, a G protein-coupled receptor known as MRGPRX2 has been identified and shown to be highly expressed on human skin but not lung mast cells. The demonstration that many NMBDs induce degranulation in human mast cells via MRGPRX2 led to the idea that this receptor contributes to NMBD-induced hypersensitivity reactions. However, other studies have raised doubts regarding its role in drug-induced hypersensitivity. This review discusses the current status and controversy on MRGPRX2's role on NMBD-induced hypersensitivity.
摘要
过敏反应是由多种触发因素引起的，包括食品和药物管理局（FDA）批准的抗生素、造影剂和神经肌肉阻断药物（NMBDs）。传统上，药物引起的过敏反应被认为主要是由于 IgE 介导的肥大细胞中组胺的释放。最近，一种被称为 MRGPRX2 的 G 蛋白偶联受体被鉴定出来，并被证明在人类皮肤而非肺肥大细胞上高度表达。许多 NMBD 通过 MRGPRX2 诱导人类肥大细胞脱颗粒的证明导致了这样一种观点，即该受体有助于 NMBD 引起的过敏反应。然而，其他研究对其在药物引起的过敏反应中的作用提出了质疑。本文讨论了 MRGPRX2 在 NMBD 引起的过敏反应中的作用的现状和争议。
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