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앰菲瑞古林通过AREG/EGFR通路促进激活调节性T细胞抑制功能,用于喉状细胞癌

Hang Li^1,2, Ruihua Fang¹, Renqiang Ma¹

¹Department of Otorhinolaryngology Head and Neck Surgery, the First Affiliated Hospital, Sun Yat-Sen University, 2nd Zhongshan Road 58#, Guangzhou, 510080, Guangdong, P.R. China.

Head & face medicine

|October 26, 2024

概括

氨基素 (AREG) 在喉平细胞癌 (LSCC) 中促进免疫抑制激活调节性T细胞 (aTregs) 的生成. 向AREG可能通过克服瘤诱导的免疫抑制来为LSCC提供一种新的免疫治疗策略.

科学领域:

免疫学免疫学免疫学
在瘤学瘤学.
癌症研究癌症研究

背景情况:

激活的调节性T细胞 (aTregs) 在喉状细胞癌 (LSCC) 中有助于形成支持瘤的免疫抑制微环境.
在LSCC中驱动aTreg生成的具体因素在很大程度上是未知的.
这项研究调查了安菲雷古林 (AREG) 在与LSCC相关的aTreg产生中的作用.

研究的目的:

阐明安菲瑞古林 (AREG) 对激活调节性T细胞 (aTregs) 诱导和功能的作用.
探索喉状细胞癌 (LSCC) 免疫疗法针对AREG/EGFR信号通路的潜力.

主要方法:

在LSCC组织中对AREG和FOXP3表达的免疫组织化学分析.
流细胞计,以评估Treg子集上的EGFR表达和AREG诱导的T细胞分化.
使用AREG和EGFR抑制剂 (Gefitinib) 的体外研究.

主要成果:

较高的AREG表达与晚期LSCC阶段相关,生存率较差,Treg透率增加.
在体外,AREG显著促进了aTreg的分化,并增强了Treg介导的免疫抑制.
抑制EGFR逆转了AREG诱导的aTreg分化和免疫抑制.
与其他Treg子集相比,EGFR在aTregs上特别受到监管.

结论:

氨基素 (AREG) 通过AREG/EGFR通路驱动LSCC中免疫抑制aTregs的生成和功能.
向AREG为喉状细胞癌提供了一个潜在的新型免疫疗法策略.
这项研究揭示了AREG在LSCC瘤微环境中的免疫逃避中的作用.

关键词:

安菲瑞古林 (Amphiregulin) 是一种氨基酸.皮肤表皮生长因子受体.免疫抑制的微环境喉皮状细胞癌的癌症.监管性T细胞监管性T细胞

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