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瘤介导的免疫抑制和细胞因子的扩散影响了EMT和PD-L1状态之间的关系

Carlijn M Lems¹, Gerhard A Burger¹, Joost B Beltman¹

¹Division of Drug Discovery and Safety, Leiden Academic Centre for Drug Research, Leiden University, Leiden, Netherlands.

Frontiers in immunology

|August 28, 2023

概括

数学模型显示,虽然编程死亡连接体1 (PD-L1) 影响T细胞,但转化生长因子β (TGFβ) 影响PD-L1的表达. 空间模拟强调了单细胞分析对于理解瘤进展的重要性.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
计算生物学计算生物学

背景情况:

表皮-介质细胞过渡 (EMT) 和编程死亡体1 (PD-L1) 是瘤进展的关键驱动因素.
它们的相互作用被建议增强瘤免疫逃逸,但免疫抑制和空间异质性的作用尚不清楚.

研究的目的:

使用数学和空间模型研究EMT,PD-L1和免疫抑制之间的相互作用.
描述细胞因子介导作用和内异质性对瘤进展和免疫逃避的影响.

主要方法:

开发了数学模型,包括PD-L1对T细胞的影响和TGFβ介导的EMT.
采用多级空间模拟来建模细胞因子异质性和内异质性.
在人群和单细胞水平上分析了EMT状态,PD-L1表达和免疫反应之间的关系.

主要成果:

通过PD-L1介导的免疫抑制极小地改变了EMT状态之间的PD-L1水平差异.
在EMT表型中,TGFβ介导的抑制导致TGFβ和PD-L1之间的负相关性.
干扰素 (IFNγ) 诱导的部分EMT对旁观细胞提供了有限的保护.
种群层面的分析可以掩盖EMT和PD-L1之间的真正关系,强调单细胞分析.

结论:

这项研究阐明了EMT和免疫逃避机制之间的复杂相互作用.
这些发现强调了单细胞分析的必要性,以准确评估EMT和PD-L1状态.
结果为开发向癌症诊断和治疗提供了关键的见解.

关键词:

在PD-L1中.细胞波茨模型的模型.表皮细胞-介质细胞过渡 (EMT)免疫逃生免疫逃生常规微分方程常规微分方程

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