免疫抑制瘤微环境和在黑色素瘤骨转移中免疫治疗的进步
Yiqun Ma1, Lin Zhang2, Weimin Liu3
1Department of Burns and Plastic Surgery, Kunming Children's Hospital, Children's Hospital Affiliated to Kunming Medical University, Kunming, China.
Frontiers in immunology
|September 12, 2025
概括
黑色素瘤骨转移是由瘤微环境 (TME) 和免疫抑制细胞驱动的. 了解这些机制是克服免疫检查点抑制剂 (ICI) 等免疫疗法耐药性的关键.
科学领域:
- 在瘤学瘤学.
- 免疫学 免疫学 免疫学
- 骨生物学 骨生物学
背景情况:
- 黑色素瘤经常转移到骨,导致严重的发病率和死亡率.
- 瘤微环境 (TME) 对黑色素瘤的进展,骨转移和对治疗的耐药性至关重要.
- 在TME内的免疫抑制细胞,包括髓质衍生抑制细胞 (MDSC),瘤相关巨细胞 (TAM),调节性T细胞 (Tregs) 和癌症相关纤维细胞 (CAF),促进免疫逃避和骨破坏.
研究的目的:
- 审查TME在黑色素瘤骨转移和免疫疗法耐药性的作用.
- 探索免疫抑制细胞驱动骨解质骨破坏的机制.
- 讨论当前和新兴的黑色素瘤免疫治疗策略.
主要方法:
- 文献综述综合了有关黑色素瘤骨转移的当前知识.
- 分析TME,免疫抑制细胞和骨破坏之间的相互作用.
- 免疫检查点抑制剂 (ICI) 和新型组合疗法的评估.
主要成果:
- TME通过RANKL依赖和独立的途径促进黑色素瘤骨转移.
- 免疫抑制细胞在骨微环境中协调免疫逃避和骨解.
- 对当前ICI (抗CTLA-4,抗PD-1/PD-L1) 的耐药性通常与TME介导的免疫抑制有关.
结论:
- 准TME对于改善黑色素瘤治疗结果至关重要.
- 旨在调节TME的组合疗法有望克服免疫疗法耐药性.
- 对TME动态的进一步研究对于开发更有效的黑色素瘤治疗方法至关重要.
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