产热
瘦素
生物
内分泌学
褐色脂肪组织
内科学
脂肪组织
小鼠苗条素受体
脂肪因子
交感神经系统
炎症
受体
肥胖
人口
医学
血压
环境卫生
作者
Emma Haberman,Gitalee Sarker,Bernardo A. Arús,Karin A. Ziegler,S Meunier,Noelia Martínez-Sánchez,Eliška Freibergerová,Sinem Yilmaz-Özcan,Iara Fernández-González,Chloe Zentai,C O'Brien,David E. Grainger,Davi Sidarta-Oliveira,Svetoslav Chakarov,Andrea Raimondi,Matteo Iannacone,Stefan Engelhardt,José Miguel Túñez López,Florent Ginhoux,Ana I. Domingos
出处
期刊:Immunity
[Elsevier]
日期:2023-12-01
被引量:1
标识
DOI:10.1016/j.immuni.2023.11.006
摘要
Adipose tissues (ATs) are innervated by sympathetic nerves, which drive reduction of fat mass via lipolysis and thermogenesis. Here, we report a population of immunomodulatory leptin receptor-positive (LepR+) sympathetic perineurial barrier cells (SPCs) present in mice and humans, which uniquely co-express Lepr and interleukin-33 (Il33) and ensheath AT sympathetic axon bundles. Brown ATs (BATs) of mice lacking IL-33 in SPCs (SPCΔIl33) had fewer regulatory T (Treg) cells and eosinophils, resulting in increased BAT inflammation. SPCΔIl33 mice were more susceptible to diet-induced obesity, independently of food intake. Furthermore, SPCΔIl33 mice had impaired adaptive thermogenesis and were unresponsive to leptin-induced rescue of metabolic adaptation. We therefore identify LepR+ SPCs as a source of IL-33, which orchestrate an anti-inflammatory BAT environment, preserving sympathetic-mediated thermogenesis and body weight homeostasis. LepR+IL-33+ SPCs provide a cellular link between leptin and immune regulation of body weight, unifying neuroendocrinology and immunometabolism as previously disconnected fields of obesity research.
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