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- W4284708730 abstract "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. Using rat and mouse models of pulmonary hypertension and patients’ data, Shu, Liu, Zhou et al. show that the concomitant increase in immunoglobulin E (IgE) and mast cells expressing the effector receptor FcεRIα has an important role in pulmonary vascular remodeling, and genetic and pharmacological inhibition of the IgE–FcεRIα signaling alleviated the progression of pulmonary hypertension in animal models." @default.
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- W4284708730 date "2022-07-07" @default.
- W4284708730 modified "2023-10-14" @default.
- W4284708730 title "Inhibition of immunoglobulin E attenuates pulmonary hypertension" @default.
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- W4284708730 doi "https://doi.org/10.1038/s44161-022-00095-9" @default.
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