过敏反应
肥大细胞
免疫球蛋白E
免疫学
TRPV1型
体温过低
脱颗粒
化学
生物
过敏
内分泌学
内科学
医学
受体
抗体
瞬时受体电位通道
作者
Chunjing Bao,Ouyang Chen,Huaxin Sheng,Jeffrey Zhang,Yikai Luo,Byron W. Hayes,Han Liang,Wolfgang Liedtke,Ru-Rong Ji,Soman N. Abraham
出处
期刊:Science immunology
[American Association for the Advancement of Science (AAAS)]
日期:2023-03-17
卷期号:8 (81)
被引量:4
标识
DOI:10.1126/sciimmunol.adc9417
摘要
IgE-mediated anaphylaxis is an acute life-threatening systemic reaction to allergens, including certain foods and venoms. Anaphylaxis is triggered when blood-borne allergens activate IgE-bound perivascular mast cells (MCs) throughout the body, causing an extensive systemic release of MC mediators. Through precipitating vasodilatation and vascular leakage, these mediators are believed to trigger a sharp drop in blood pressure in humans and in core body temperature in animals. We report that the IgE/MC-mediated drop in body temperature in mice associated with anaphylaxis also requires the body’s thermoregulatory neural circuit. This circuit is activated when granule-borne chymase from MCs is deposited on proximal TRPV1 + sensory neurons and stimulates them via protease-activated receptor-1. This triggers the activation of the body’s thermoregulatory neural network, which rapidly attenuates brown adipose tissue thermogenesis to cause hypothermia. Mice deficient in either chymase or TRPV1 exhibited limited IgE-mediated anaphylaxis, and, in wild-type mice, anaphylaxis could be recapitulated simply by systemically activating TRPV1 + sensory neurons. Thus, in addition to their well-known effects on the vasculature, MC products, especially chymase, promote IgE-mediated anaphylaxis by activating the thermoregulatory neural circuit.
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