CCL22型
趋化因子
产热
脂肪组织
CXCL10型
趋化因子受体
细胞生物学
生物
脂肪细胞
内分泌学
免疫学
炎症
作者
Yexian Yuan,Ruoci Hu,Jooman Park,Shaolei Xiong,Zilai Wang,Yanyu Qian,Zuoxiao Shi,Ruifan Wu,Zhenbo Han,Sang‐Ging Ong,Shuhao Lin,Krista A Varady,Pingwen Xu,Daniel C. Berry,Gang Shu,Yuwei Jiang
出处
期刊:Science Advances
[American Association for the Advancement of Science (AAAS)]
日期:2024-06-26
卷期号:10 (26)
被引量:1
标识
DOI:10.1126/sciadv.adn5229
摘要
There is a regional preference around lymph nodes (LNs) for adipose beiging. Here, we show that local LN removal within inguinal white adipose tissue (iWAT) greatly impairs cold-induced beiging, and this impairment can be restored by injecting M2 macrophages or macrophage-derived C-C motif chemokine (CCL22) into iWAT. CCL22 injection into iWAT effectively promotes iWAT beiging, while blocking CCL22 with antibodies can prevent it. Mechanistically, the CCL22 receptor, C-C motif chemokine receptor 4 (CCR4), within eosinophils and its downstream focal adhesion kinase/p65/interleukin-4 signaling are essential for CCL22-mediated beige adipocyte formation. Moreover, CCL22 levels are inversely correlated with body weight and fat mass in mice and humans. Acute elevation of CCL22 levels effectively prevents diet-induced body weight and fat gain by enhancing adipose beiging. Together, our data identify the CCL22-CCR4 axis as an essential mediator for LN-controlled adaptive thermogenesis and highlight its potential to combat obesity and its associated complications.
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