Inhibition of immunoglobulin E attenuates pulmonary hypertension

抗体 医学 肺动脉高压 免疫学 心脏病学 内科学
作者
Ting Shu,Ying Liu,Yitian Zhou,Zhou Zhou,Bolun Li,Yanjiang Xing,Peiran Yang,Junling Pang,Jinqiu Li,Xiaomin Song,Xin Ning,Xianmei Qi,Chang-ming Xiong,Hang Yang,Qianlong Chen,Jingyu Chen,Ying Yu,Jing Wang,Chen Wang
出处
期刊:Nature Cardiovascular Research [Springer Nature]
卷期号:1 (7): 665-678 被引量:5
标识
DOI:10.1038/s44161-022-00095-9
摘要

Pulmonary hypertension (PH) is a severe cardiopulmonary disease characterized by pulmonary vascular remodeling. Immunoglobulin E (IgE) is known to participate in aortic vascular remodeling, but whether IgE mediates pulmonary vascular disease is unknown. In the present study, we found serum IgE elevation in pulmonary arterial hypertension (PAH) patients, hypoxia-induced PH mice and monocrotaline-induced PH rats. Neutralizing IgE with an anti-IgE antibody was effective in preventing PH development in mice and rat models. The IgE receptor FcεRIα was also upregulated in PH lung tissues and Fcer1a deficiency prevented the development of PH. Single-cell RNA-sequencing revealed that FcεRIα was mostly expressed in mast cells (MCs) and MC-specific Fcer1a knockout protected against PH in mice. IgE-activated MCs produced interleukin (IL)-6 and IL-13, which subsequently promoted vascular muscularization. Clinically approved IgE antibody omalizumab alleviated the progression of established PH in rats. Using genetic and pharmacological approaches, we have demonstrated that blocking IgE-FcεRIα signaling may hold potential for PAH treatment.
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