IL-6信号驱动脂肪组织巨细胞的自我更新和替代激活
Jan Ackermann1,2, Lilli Arndt1,2, Janine Fröba1
1Institute of Anatomy, Leipzig University, Leipzig, Germany.
Frontiers in immunology
|March 14, 2024
概括
干白素-6 (IL-6) 减少炎症并维持脂肪组织中的巨细胞增殖,独立于IL-4Rα信号传递. 这表明IL-6在控制与肥胖相关的炎症和巨细胞动态方面发挥着关键作用.
科学领域:
- 免疫学 免疫学 免疫学
- 代谢性疾病研究研究
- 细胞生物学 细胞生物学
背景情况:
- 肥胖与慢性脂肪组织 (AT) 炎症和AT巨细胞 (ATM) 增加有关,有助于2型糖尿病.
- 之前的研究表明,中和介质素-6 (IL-6) 抑制了肥胖AT器官培养中的ATM增殖,有利于替代激活的表型.
研究的目的:
- 研究IL-6信号传递在脂肪组织 (AT) 生物学和代谢表型中的作用.
- 在小鼠中检查AT炎症,ATM极化和扩散,这些小鼠具有髓状细胞特异性IL-6受体α (IL-6Rα) 缺乏 (Il6raΔmyel).
主要方法:
- 在正常食和高脂肪饮食中的Il6raΔmyel小鼠中研究了AT生物学和代谢表型.
- 利用来自IL-4Rα淘汰小鼠 (Il4ra-/-) 的器官型AT培养和骨髓衍生巨细胞 (BMDM) 来研究IL-6信号通路.
主要成果:
- 肥胖的Il6raΔmyel小鼠在胰岛素敏感性或AT炎症标志物中没有显著差异.
- 在Il6raΔmyel小鼠中观察到CD206+ATM和Ki67+增殖ATM的减少.
- IL-6促进向M2巨细胞表型的转变,独立于IL-6/IL-4Rα轴,正如AT培养和BMDMs所示.
结论:
- IL-6对巨细胞具有独立于IL-4Rα的抗炎作用.
- IL-6对于维持肥胖脂肪组织内的巨细胞增殖率至关重要.
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