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为什么免疫"检查点"治疗在大多数临床试验中失败了?

Xuan Yang¹, Lieping Chen^2,3,4

¹Department of Immunobiology, Yale School of Medicine, New Haven, Connecticut, USA.

Journal for immunotherapy of cancer

|August 27, 2025

概括

尽管PD-1/PD-L1途径抑制剂取得了成功,但其他检查点抑制剂如TIM-3和TIGIT的效果有限. 这篇评论探讨了这些失败的原因,并提出了癌症免疫治疗的战略路径.

科学领域:

免疫学
癌症学
药理学

背景情况:

使用PD-1/PD-L1通路阻塞的癌症免疫疗法在各种癌症中取得了显著的临床成功.
针对TIM-3和TIGIT等分子的其他免疫检查点抑制剂的开发也带来了有限的临床益处,即使是在组合疗法中.

研究的目的:

探索解释免疫检查点抑制剂差异性治疗成功的关键假设.
为推进癌症免疫疗法提供生物知识的策略.

主要方法:

审查精选的证据和科学文献.
对检查点抑制剂有效性的三个核心假设的探索.
对瘤微环境 (TME) 免疫逃避机制的分析.

主要成果:

假设1:许多检查点目标缺乏瘤特异性的免疫抑制功能.
假设2:TME中的免疫逃避机制是主导的,但不是多余的.
假设3:获得的耐药性在治疗过程中出现.

结论:

新型检查点抑制剂的有限成功可能源于它们的点生物和复杂的TME.
考虑瘤特异性免疫抑制,TME动态和抵抗机制的更战略性方法对于未来的癌症免疫疗法发展至关重要.

关键词:

免疫调节免疫抑制免疫疗法瘤微环境 - - 瘤微环境

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