与瘤相关的巨细胞重塑抑制瘤的免疫微环境,并针对免疫疗法进行向治疗
Yan Yang1, Sijia Li1, Kenneth K W To2
1State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, P. R. China.
概括
瘤微环境 (TME) 中的瘤相关巨细胞 (TAM) 驱动癌症免疫逃避和免疫治疗耐药性. 针对TAM及其相互作用提供了一个有希望的策略,以提高癌症免疫治疗的有效性.
科学领域:
- 免疫学 免疫学 免疫学
- 在瘤学瘤学.
- 癌症研究 癌症研究
背景情况:
- 免疫检查点抑制剂 (ICI) 在癌症免疫治疗中表现有前途,但耐药性仍然是一个重大挑战.
- 在瘤微环境 (TME) 内的瘤相关巨细胞 (TAMs) 极大地影响瘤进展和免疫逃避.
- TAMs调节M1/M2巨细胞平衡并产生免疫抑制的TME,有助于免疫治疗耐受性.
研究的目的:
- 系统地审查TAMs的起源,功能性可塑性和两极化.
- 阐明TAMs和其他TME组件在驱动瘤启动,进展和免疫逃避方面的复杂相互作用.
- 通过调查TAM-TME通信网络来确定优化癌症免疫治疗的新型分子标.
主要方法:
- 对TAMs,巨细胞极化和TME相互作用的当前文献进行系统审查.
- 分析调节巨细胞极化和TAM功能的关键信号通路.
- 探索TAM与TME内的其他细胞和非细胞组成部分之间的交叉通话.
主要成果:
- TAMs在塑造免疫抑制性TME中发挥着关键作用,促进瘤生长和免疫逃避.
- 了解TAM信号通路及其与TME的相互作用对于克服ICI电阻至关重要.
- TAM异质性和可塑性带来了挑战,但也为有针对性的治疗策略提供了机会.
结论:
- 向TAM及其在TME中的相互作用具有显著的潜力,可以提高癌症免疫治疗的疗效.
- 需要进一步的研究来解码复杂的TAM-TME相互作用,并将临床前发现转化为临床应用.
- 解决TAM异质性,可塑性和耐药性机制对于在TAM向治疗中实现最佳临床结果至关重要.
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