补充成分3链接在过敏性鼻炎中表皮重塑和巨代谢重编程
Xuan Yuan1, Shaobing Xie1, Liyuan Liu2
1Division of Allergy and Clinical Immunology, Johns Hopkins University School of Medicine, Baltimore, MD, 21224, USA; Department of Otolaryngology Head and Neck Surgery, Xiangya Hospital of Central South University, Changsha, Hunan, 410008, China.
The Journal of allergy and clinical immunology
|February 27, 2026
概括
补充成分3 (C3) 和它的受体 (C3aR) 信号驱动过敏性鼻炎通过重编程巨细胞脂质代谢来进行表皮重塑. 这一途径加剧了基底细胞增生和炎症.
科学领域:
- 免疫学 免疫学 免疫学
- 过敏性炎症 过敏性炎症
- 皮质生物学 皮质生物学
背景情况:
- 过敏性鼻炎 (AR) 的特征是上皮重塑,特别是基底细胞增生.
- 与AR相关的上游表皮质重塑的驱动因素和机制尚未完全理解.
研究的目的:
- 研究补充成分3 (C3) 和C3a-C3a受体 (C3aR) 信号传导在AR上皮层重塑中的作用.
- 探索C3/C3aR信号对巨细胞介导炎症和AR中的代谢重编程的影响.
主要方法:
- 从AR患者和对照对鼻腔粘膜的转录组测序.
- 对AR患者的上皮重塑的评估,小鼠模型和细胞培养.
- 使用C3缺乏的小鼠和C3aR抗剂来评估C3/C3aR信号效应.
- 研究脂肪酸氧化 (FAO) 和PCCB在巨细胞激活中的作用.
主要成果:
- 鼻腔粘膜的AR显示表皮重塑和基底细胞增生增加.
- 在AR粘膜中,C3是最大程度上调的补充基因,与疾病严重程度相关.
- 缺乏C3或C3aR对抗性减少了AR相关的表皮重塑,增生和炎症.
- C3a-C3aR信号传递促进了具有脂质代谢程序的CD206+巨细胞.
- 抑制粮农组织或PCCB减弱的C3aR驱动的巨细胞激活和随后通过TGF-β1.1.进行表皮重塑.
结论:
- 在过敏性鼻炎中,C3/C3a-C3aR信号传递是表皮质重塑的关键驱动因素.
- 这种信号通路促进了巨细胞的脂质代谢重编程,有助于AR的发病.
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