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:Designing Cancer Immunotherapies That Engage T Cells and NK Cells.
Designing Cancer Immunotherapies That Engage T Cells and NK Cells.
分数与星级只用于站内排序 —— 不代表疗效、安全性或个人适用性。
T 细胞和自然杀伤(NK)细胞在肿瘤免疫中具有互补作用,因此 T 细胞和 NK 细胞的双重攻击为深化免疫治疗的影响提供了机会。近期研究还表明,NK 细胞在将树突状细胞募集到肿瘤中发挥重要作用,从而增强 CD8 T 细胞应答的诱导,而 T 细胞分泌的 IL-2 则激活 NK 细胞。靶向来自活化性 NKG2D 受体及其在肿瘤细胞上的 MICA 和 MICB 配体的免疫逃逸机制,为治疗干预提供了机会。有趣的是,T 细胞和 NK 细胞共享若干重要的抑制性和活化性受体,可靶向这些受体以增强 T 细胞和 NK 细胞介导的免疫。这些抑制性受体-配体系统包括 CD161-CLEC2D、TIGIT-CD155 和 NKG2A/CD94-HLA-E。我们还讨论了基于抑制性和活化性细胞因子的新兴治疗策略,这些细胞因子深刻影响肿瘤内两种淋巴细胞群体的功能。
T cells and natural killer (NK) cells have complementary roles in tumor immunity, and dual T cell and NK cell attack thus offers opportunities to deepen the impact of immunotherapy. Recent work has also shown that NK cells play an important role in recruiting dendritic cells to tumors and thus enhance induction of CD8 T cell responses, while IL-2 secreted by T cells activates NK cells.
Targeting of immune evasion mechanisms from the activating NKG2D receptor and its MICA and MICB ligands on tumor cells offers opportunities for therapeutic intervention. Interestingly, T cells and NK cells share several important inhibitory and activating receptors that can be targeted to enhance T cell- and NK cell-mediated immunity. These inhibitory receptor-ligand systems include CD161-CLEC2D, TIGIT-CD155, and NKG2A/CD94-HLA-E.
We also discuss emerging therapeutic strategies based on inhibitory and activating cytokines that profoundly impact the function of both lymphocyte populations within tumors.
在 PubMed 查看 → 出版商原文(DOI) 全文 PDF(PMC)· 可下载 治疗专题与资料阅读指南 资料来源与翻译说明 报告译文或资料问题 →
MEMBER ACCOUNT
登录成功会直接打开下一页。