瘤免疫:效应因子对瘤的反应以及微环境的作用
Alberto Mantovani1, Pedro Romero, A Karolina Palucka
1Istituto Clinico Humanitas and Institute of Pathology, University of Milan, Milan, Italy.
Lancet (London, England)
|February 16, 2008
概括
矛盾的是,炎症可以促进或对抗癌症. 合成分子模仿病原体入侵激活免疫细胞,触发癌细胞的破坏,并放大针对已建立瘤的抗癌反应.
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:
- 炎症在癌症中起着双重作用,促进瘤发生,有时促进癌症排斥.
- 从促癌变向抗癌炎症的转换模仿了病原体感染反应.
- 癌症通常缺乏危险信号,阻碍有效的免疫反应.
研究的目的:
- 探索炎症在癌症中的双重作用背后的机制.
- 研究将促癌炎症转化为抗癌免疫的策略.
- 评估合成分子作为癌症免疫疗法.
主要方法:
- 分析癌症炎症的临床和实验观察结果.
- 开发模仿病原体危险信号的合成分子.
- 研究树突细胞的激活和随后的免疫反应.
主要成果:
- 合成分子激活树突细胞,产生诱导癌细胞死亡的细胞因子.
- 死亡的癌细胞提供抗原,导致抗原特异性T和B细胞的激活.
- 这一过程放大了抗癌炎症反应.
结论:
- 虽然抗炎药物可以预防一些癌症,但积极免疫与瘤微环境激活相结合,对治疗已存在的癌症有很大的希望.
- 合成分子可以将炎症重定向到破坏癌症.
- 通过有针对性的激活利用免疫反应是癌症治疗的关键策略.
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