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Updated: Jan 14, 2026

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牙周炎促进OSCC和前列腺癌的进展和免疫抑制,通过歪曲HSPC的髓状分化来抑制免疫抑制
1Department of Periodontology, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Research Center of Dental Materials and Oral Tissue Regeneration & Shandong Provincial Clinical Research Center for Oral Diseases, Jinan, Shandong, China.
Journal of dental research
|October 18, 2025
概括
牙周炎通过创建免疫抑制瘤微环境来促进癌症. 这涉及骨髓中由炎症驱动的骨髓细胞扩张,可以向减少癌症进展.
科学领域:
- 在瘤学瘤学.
- 免疫学 免疫学 免疫学
- 牙周病学 牙周病学
背景情况:
- 炎症是癌症发展的关键因素.
- 流行病学研究表明牙周炎与癌症风险之间存在联系,但机制尚不清楚.
研究的目的:
- 研究牙周炎影响癌症进展和瘤微环境的机制.
- 探索系统性炎症和骨髓改变在牙周炎相关癌症中的作用.
主要方法:
- 口腔状细胞癌和前列腺癌的小鼠模型.
- 对瘤微环境,免疫细胞群 (MDSCs,TAMs,T细胞) 和骨髓造血干细胞和祖先细胞的分析.
- 研究了互白素-1 (IL-1) 信号传递的作用.
主要成果:
- 牙周炎促进了癌症的进展,并培养了免疫抑制性瘤微环境 (iTME),其中包括扩展的髓质衍生抑制细胞 (MDSC),瘤相关的巨细胞和调节性T细胞.
- 牙周炎增强了MDSC免疫抑制功能,并减少了CD8+ T细胞透.
- 牙周炎引起的系统性炎症在骨髓中诱导了骨髓偏向的血液形成,通过IL-1信号增加了骨髓细胞的产生.
结论:
- 牙周炎远程诱导血造干细胞和祖细胞中的髓状偏差.
- 牙周炎和骨髓之间的IL-1介导轴是促进瘤发育和iTME建立的关键机制.
- 在骨髓中准IL-1R1可以减弱牙周炎诱导的瘤增长,并改善TME.
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