J Exp Med :吕建新/吕志民团队合作揭示胶质瘤母细胞免疫逃逸新机制

2020-09-03 BW Bio生物世界

胶质母细胞瘤是一类常见的原发性恶性脑肿瘤。由于这类肿瘤恶性程度极高,所以绝大部分的患者预后极差:胶质母细胞瘤患者经过手术放化疗等治疗手段后,其生存中位数仅为14个月左右,五年生存率仍不到5%。

胶质母细胞瘤(glioblastoma multiforme,GBM)是一类常见的原发性恶性脑肿瘤。由于这类肿瘤恶性程度极高,所以绝大部分的患者预后极差:胶质母细胞瘤患者经过手术放化疗等治疗手段后,其生存中位数仅为14个月左右,五年生存率仍不到5%,因此胶质母细胞瘤是当今肿瘤治疗中的重大挑战之一。随着肿瘤免疫治疗技术的进步与发展,给胶质母细胞瘤的治疗带来了新的希望。

温州医科大学吕建新团队与浙江大学转化医学研究院吕志民团队合作,在 Journal of Experimental Medicine 杂志在线发表了题为:β-catenin induces transcriptional expression of PD-L1 to promote glioblastoma immune evasion 的研究论文。

该研究发现了胶质母细胞瘤中激活异常的AKT/β-catenin信号会导致免疫检查点分子PD-L1表达水平升高并造成肿瘤免疫逃逸。基于该研究结果,研究人员使用AKT抑制剂MK2206与PD-1抗体联合用药治疗小鼠胶质母细胞瘤模型,发现联合用药对胶质母细胞瘤模型的治疗效果远好于单药治疗。

肿瘤细胞逃避免疫系统攻击的手段多样,其中较为常见的是产生一个不利于免疫细胞发挥杀伤作用的微环境和上调自身免疫抑制分子的表达水平等。

PD-L1是由CD274编码的免疫抑制分子,它能通过与T细胞表面的PD-1结合,并导致T细胞的增殖、激活和杀伤能力等受到抑制。大量文献报道在肿瘤中PD-L1的表达水平显着高于癌旁组织,同时PD-L1水平越高也预示着更为糟糕的预后。

研究团队发现胶质瘤标本中激活的β-catenin水平与PD-L1表达水平呈正相关,而与肿瘤组织中浸润的CD8+T细胞数呈负相关;进一步研究发现Wnt通路和EGFR通路激活均可促使β-catenin激活,随后β-catenin与TCF/LEF形成复合物并结合到CD274基因的启动子上,从而引起PD-L1的表达水平升高;同时,研究人员还发现AKT介导了Wnt通路和EGFR通路对β-catenin/CD274的调控作用。

在后续的研究中,他们将PD-1抗体与已进入临床二期的AKT抑制剂MK2206联合用药治疗小鼠同种原位胶质母细胞瘤模型,研究表明联合用药不但能更有效地促进肿瘤中CD8+T细胞的浸润水平,同时还能更显着地延长荷瘤小鼠的生存期。

该研究率先揭示了肿瘤中AKT/β-catenin通路对免疫检查点PD-L1调控的机制,并提出了使用AKT抑制剂与PD-1抗体联合用药治疗胶质母细胞瘤的新策略,具有较高的临床转化价值。

原始出处:

Linyong Du, Jong-Ho Lee, Hongfei Jiang,et al.β-Catenin induces transcriptional expression of PD-L1 to promote glioblastoma immune evasion.J Exp Med. 2020 Nov 2;217(11):e20191115. doi: 10.1084/jem.20191115.

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    2020-12-08 147704a8m86暂无昵称

    !牛

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    2020-09-03 金黎明

    意思是用PD-1联合治疗效果好吗?

    0

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    2020-09-03 肿肿

    机制研究离临床仍然有距离,不过与临床结合思考,仍然有帮助的,不能仅仅是纯临床思维,转化思维同样重要

    0

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    2020-09-03 火炎魂

    0

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    2020-09-03 1e0e5a1fm42(暂无匿称)

    很好

    0

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