Thapaliya Monica, Chompunud Na Ayudhya Chalatip, Amponnawarat Aetas, Roy Saptarshi, Ali Hydar
Department of Basic and Translational Sciences, University of Pennsylvania, School of Dental Medicine, Philadelphia, PA, 19104, USA.
Curr Allergy Asthma Rep. 2021 Jan 4;21(1):3. doi: 10.1007/s11882-020-00979-5.
Atopic dermatitis (AD) and allergic asthma are complex disorders with significant public health burden. This review provides an overview of the recent developments on Mas-related G protein-coupled receptor-X2 (MRGPRX2; mouse counterpart MrgprB2) as a potential candidate to target neuro-immune interaction in AD and allergic asthma.
Domestic allergens directly activate sensory neurons to release substance P (SP), which induces mast cell degranulation via MrgprB2 and drives type 2 skin inflammation in AD. MRGPRX2 expression is upregulated in human lung mast cells and serum of asthmatic patients. Both SP and hemokinin-1 (HK-1 generated from macrophages, bronchial cells, and mast cells) cause degranulation of human mast cells via MRGPRX2. MrgprB2 contributes to mast cell-nerve interaction in the pathogenesis of AD. Furthermore, asthma severity is associated with increased MRGPRX2 expression in mast cells. Thus, MRGPRX2 could serve as a novel target for modulating AD and asthma.
特应性皮炎（AD）和过敏性哮喘是具有重大公共卫生负担的复杂疾病。本综述概述了与Mas相关的G蛋白偶联受体X2（MRGPRX2；小鼠对应物为MrgprB2）作为靶向AD和过敏性哮喘中神经免疫相互作用的潜在候选物的最新进展。
室内变应原直接激活感觉神经元以释放P物质（SP），SP通过MrgprB2诱导肥大细胞脱颗粒，并驱动AD中的2型皮肤炎症。MRGPRX2在人肺肥大细胞和哮喘患者血清中的表达上调。SP和血激肽-1（由巨噬细胞、支气管细胞和肥大细胞产生的HK-1）均通过MRGPRX2导致人肥大细胞脱颗粒。MrgprB2在AD发病机制中有助于肥大细胞与神经的相互作用。此外，哮喘严重程度与肥大细胞中MRGPRX2表达增加有关。因此，MRGPRX2可作为调节AD和哮喘的新靶点。
