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由hiPSC衍生的内皮细胞和心肌细胞对参与免疫检查点抑制剂相关心肌炎的细胞因子的明显炎症反应
Samantha Conte1,2,3, Isaure Firoaguer1,2,3, Simon Lledo1,2,3
1Aix Marseille Univ, Inserm, INRAE, C2VN, 13005 Marseille, France.
Cells
|September 13, 2025
概括
免疫检查点抑制剂诱导心肌炎 (ICI-M) 涉及细胞因子的升高. 人类干细胞模型显示内皮细胞比心肌细胞更容易受到这些炎症性细胞因子的影响,这表明内皮功能障碍是ICI-M的关键.
科学领域:
- 心脏病学 心脏病学
- 免疫学 免疫学 免疫学
- 干细胞生物学 干细胞生物学
背景情况:
- 免疫检查点抑制剂诱导的心肌炎 (ICI-M) 与干扰素-γ (IFN-γ) 和炎症酶激活等炎症性细胞因子的升高有关.
- 在ICI-M病理生理学中,特定的细胞点和这些因素的相互作用尚未得到充分理解.
研究的目的:
- 研究ICI-M相关细胞因子对人类诱导多能干细胞 (hiPSC) 衍生内皮细胞 (EC) 和心肌细胞 (CM) 的活力和炎症反应的影响.
主要方法:
- 由hiPSC衍生的EC和CM暴露于IFN-γ或细胞因子尾酒.
- 使用微阵列分析了转录组变化.
- 评估了与炎症,细胞亡和细胞死亡相关的细胞和分子通路.
主要成果:
- 在暴露于细胞因子时,hiPSC-ECs表现出显著的死亡率和免疫和炎症途径的明显转录组变化.
- hiPSC-CMs显示出有限的转录性改变和较低的对细胞因子诱导死亡的敏感性.
- 细胞因子治疗在两种细胞类型中调高了炎症组分 (例如,GBP5,AIM2,GSDMD),增加了GBP5和分裂的CASP-1,反映了患者活检的结果.
结论:
- 与心肌细胞相比,内皮细胞对与ICI-M相关的炎症具有更高的脆弱性.
- 由炎性酶激活驱动的内皮功能障碍,在ICI-M中成为一个中心机制.
- 向内皮炎症酶途径,如AIM2抑制,可能提供一种治疗策略,以减轻ICI治疗引起的心脏毒性.
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