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
NK 细胞对人致癌γ-疱疹病毒感染的应答
英文原题：Natural killer cell responses to human oncogenic γ-herpesvirus infections.
查看英文原题
Natural killer cell responses to human oncogenic γ-herpesvirus infections.
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中文摘要
两种γ-疱疹病毒Epstein Barr病毒（EBV）和Kaposi肉瘤相关疱疹病毒（KSHV）各自与人类所有肿瘤中超过1%的肿瘤相关。虽然EBV在几乎所有成年个体中建立持续性感染，但KSHV受益于EBV的广泛流行以实现自身的持续存在。有趣的是，EBV感染扩增了早期分化的NKG2A + KIR - NK细胞，这些细胞可防止裂解性EBV感染，而KSHV共感染则驱动功能低下的CD56 - CD16 + NK细胞积聚。因此，持续性γ-疱疹病毒感染是人类NK细胞库的塑造者，各自刺激的NK细胞亚群应考虑用于EBV和KSHV相关恶性肿瘤的免疫治疗。
展开英文摘要原文
The two γ-herpesviruses Epstein Barr virus (EBV) and Kaposi sarcoma associated herpesvirus (KSHV) are each associated with more than 1% of all tumors in humans. While EBV establishes persistent infection in nearly all adult individuals, KSHV benefits from this widespread EBV prevalence for its own persistence. Interestingly, EBV infection expands early differentiated NKG2A + KIR - NK cells that protect against lytic EBV infection, while KSHV co-infection drives accumulation of poorly functional CD56 - CD16 + NK cells.
Thus persistent γ-herpesvirus infections are sculptors of human NK cell repertoires and the respectively stimulated NK cell subsets should be considered for immunotherapies of EBV and KSHV associated malignancies.
论文信息
- 作者
- Münz C
- 单位
- Viral Immunobiology, Institute of Experimental Immunology, University of Zürich, Switzerland. Electronic address: christian.muenz@uzh.ch.Switzerland
- 文献类型
- 综述 · 非美国政府资助研究
- 期刊
- Seminars in immunology2022 Mar
- 原文标识
- PubMed 36162228 · DOI 10.1016/j.smim.2022.101652