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在儿科急性淋巴细胞白血病中的Th1细胞因子

Sarah Schober¹, Jennifer M Rottenberger¹, Johannes Hilz¹

¹Department I - General Pediatrics, Hematology/Oncology, University Children's Hospital, Eberhard Karls University Tuebingen, Tuebingen, Germany.

Cancer immunology, immunotherapy : CII

|August 23, 2023

概括

Th1细胞因子,瘤亡因子α和干扰素gamma,诱导大多数儿科急性淋巴细胞白血病 (ALL) 细胞的亡. 干扰素玛受体表达和STAT1激活与细胞死亡相关,突出IFN-γ.

科学领域:

免疫学免疫学免疫学
在瘤学瘤学.
细胞生物学细胞生物学

背景情况:

免疫微环境显著影响癌症的进展.
包括TNF-α和IFN-γ在内的Th1细胞因子是关键的免疫调节剂.
儿科急性淋巴细胞白血病 (ALL) 是一种由免疫因素影响的复杂疾病.

研究的目的:

研究Th1细胞因子 (TNF-α和IFN-γ) 对儿科ALL的影响.
分析ALL细胞系和患者衍生的异种移植 (PDX) 对这些细胞因子的反应.
为了将细胞因子受体表达和细胞内信号与观察到的细胞效应相关联.

主要方法:

所有细胞系和PDX的化,TNF-α和IFN-γ的度各不相同.
细胞死亡诱导和活力的评估.
对细胞因子受体 (TNFR,IFNGR) 表达水平的分析.
测量细胞内信号分子酸化 (STAT1,NF-κB).

主要成果:

观察到ALL细胞和PDX对TNF-α和IFN-γ反应的显著异质性.
细胞亡被确定为由Th1细胞因子诱导的细胞死亡的主要机制.
IFN-γ受体 (IFNGR) 的更高表达与增加的STAT1酸化和更大的细胞死亡相关.
发现STAT1激活与Th1细胞因子刺激后的细胞死亡程度相关.

结论:

TNF-α和IFN-γ对儿科ALL细胞和PDX具有异质作用,但在大多数情况下可以诱导细胞亡.
高IFNGR表达和随后的STAT1激活与ALL细胞死亡的增加有关.
IFN-γ信号传递在调解儿科ALL的Th1细胞因子诱导的细胞死亡方面发挥着至关重要的作用.

关键词:

在INF-γ中使用.儿科急性淋巴细胞白血病患者.这就是TNF-α.Th1 细胞因子

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