RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:Epigenetic therapies for neuroblastoma: immunogenicity awakens.
Epigenetic therapies for neuroblastoma: immunogenicity awakens.
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神经母细胞瘤免疫疗法的开发仍然具有挑战性,原因在于神经母细胞瘤细胞的低免疫原性,这体现在免疫识别的主要触发因素之一——主要组织相容性复合体I类(MHC-I)的低表达上。Cornel等人表明,使用组蛋白去乙酰化酶抑制剂对神经母细胞瘤细胞进行表观遗传调控,可以增强主要组织相容性复合体I类以及其他免疫受体的表达,从而启动T细胞和NK 细胞对其的识别。通过利用神经母细胞瘤发育相关的异常表观遗传景观,这些发现为克服神经母细胞瘤免疫治疗领域的一个主要限制开辟了道路。
The development of immunotherapies for neuroblastoma remains challenging owing to the low immunogenicity of neuroblastoma cells, as reflected by the low expression of one of the main triggers of immune recognition, the major histocompatibility complex class I (MHC-I). Cornel et al.
showed that epigenetic modulation of neuroblastoma cells with a histone deacetylase inhibitor can boost the expression of major histocompatibility complex class I, among other immune receptors, priming their recognition by T- and natural killer cells. By leveraging the developmentally related aberrant epigenetic landscapes of neuroblastoma, these discoveries pave the way to overcome a major limitation in the field of neuroblastoma immunotherapy.
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