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京福康通过调节T细胞受体来抑制肺癌转移

Bin Luo¹, Panpan Wang², Jianhui Tian²

¹Clinical Oncology Center, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, 200071, Shanghai, China; Department of Oncology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, 200032, Shanghai, China.

Journal of ethnopharmacology

|July 8, 2023

概括

京福康 (JFK) 治疗通过增加有益的免疫细胞,如CD8+ T淋巴细胞和NK细胞,减少了小鼠的肺癌转移. 此外,JFK还逆转了与瘤进展相关的T细胞受体 (TCR) 基因表达变化,为治疗肺癌转移提供了新的策略.

科学领域:

免疫学免疫学免疫学
在瘤学瘤学.
药理学药理学是指药理学的学科.

背景情况:

转移是肺癌死亡的主要原因,免疫逃逸是关键因素.
京福康 (JFK) 通过调节T淋巴细胞,在治疗肺癌转移方面表现出有效性.
在肺癌转移期间,JFK在调节T细胞受体 (TCR) 的特定作用仍未被探索.

研究的目的:

为了研究JFK在肺癌中的抗转移效应.
为了确定JFK是否通过调节TCRs来抑制肺癌转移.
在肺转移模型中阐明JFK对免疫细胞群和TCR基因表达的影响.

主要方法:

使用易斯肺癌细胞在小鼠身上建立了肺转移模型.
通过连续的胃内输液给药JFK.
通过解剖学观察和血素-素染色,评估肺转移.
通过流细胞计分析免疫细胞群 (T细胞,MDSC,巨细胞).
使用免疫组织化学和免疫光学评估瘤增殖和免疫细胞透.
在外围血液和肺组织中进行了TCR多样性和基因表达分析的免疫谱系测序,随后进行了生物信息学分析.

主要成果:

肯德基治疗显著降低了肺转移性结节的数量和整体肺瘤负担.
JFK增加了CD8+ T淋巴细胞和NK细胞在肺转移组织中的透.
肯尼迪医院在外周血液中增加了CD4+ T,CD8+ T和NKT细胞的比例.
肯尼迪调节了MDSC比率,并在外周血液中增加了M1巨细胞的比例.
虽然TCR多样性保持不变,但JFK逆转了由瘤进展引起的特定TCR基因表达改变 (TRBV16,TRBV17,TRBV1的下调;TRBV12-2的上调).

结论:

通过提高周围血液中的CD4+,CD8+T和NKT细胞比例,JFK抑制肺癌转移.
JFK促进CD8+ T和NK细胞透到瘤组织中.
肯德基逆转了瘤诱导的TCR基因表达变化,这表明其抗转移效应的新机制.
这些发现支持JFK和类似的中国草药的发展,作为针对肺癌转移的TCR治疗策略.

关键词:

免疫系统的曲目.京福康 (Jinfukang) 公司肺癌是一种肺癌.转移转移转移转移 T细胞受体的T细胞受体.

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