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:The dual effect of interferon-γ in acute myeloid leukemia: A narrative review.
The dual effect of interferon-γ in acute myeloid leukemia: A narrative review.
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急性髓系白血病(AML)是一种血液系统恶性肿瘤,表现为骨髓和外周循环中髓系前体细胞非常快速、不受控制的增殖。关于AML的研究已突出显示IFN-γ治疗在免疫监视、对白血病细胞既有促进作用又有抑制作用以及调节肿瘤微环境中的关键作用。
然而,仍需全面理解IFN-γ在AML中的双重作用。因此,本综述旨在评估IFN-γ在AML中的双重作用。在PubMed、Google Scholar和直接Google搜索中进行了文献检索。数据以表格和图形呈现,并通过叙述性综合总结研究结果。根据疾病的情况和阶段,IFN-γ在AML患者中表现出两种不同的活性。首先,IFN-γ增强NK细胞和CD8+ T淋巴细胞功能,这些共同激发抗白血病免疫。IFN-γ的另一项有前景的作用包括诱导髓系细胞分化,从而可能降低白血病的严重程度。
然而,长期暴露于IFN-γ可激活Treg细胞和抑制性免疫检查点,这可能帮助白血病逃避免疫监视并进入免疫抑制环境。我们的综述强调了IFN-γ在免疫系统与AML发病机制之间复杂相互作用中的关键作用。其既抑制又促进白血病过程的双重作用已得到强调。
然而,未来的临床前和临床研究应聚焦于IFN-γ影响AML进展和治疗结局的具体机制,以期实现患者的治愈性结果。
Acute myeloid leukemia (AML) is a hematological malignancy representing a very rapid, uncontrolled growth of myeloid precursors in the BM and peripheral circulation. Studies on AML have highlighted the crucial role of IFN-γ therapy in immune surveillance, both promotive and inhibitory effects on leukemic cells, and regulation of the tumor microenvironment.
However, there is a need for a comprehensive understanding of the dual effects of IFN-γ in AML.
Thus, this review aimed to assess the dual effects of IFN-γ in AML. Literature searches were conducted in Pub Med, Google Scholar, and direct Google Search. The data was presented in tables and figures, with findings summarized through a narrative synthesis.
Depending on the circumstances and stage of the disease IFN-γ shows two different activities in AML patients. First, IFN-γ enhances NK cells and CD8 + T lymphocyte functions, which collectively evoke antileukemic immunity. Another promising effect of IFN-γ includes the differentiation of myeloid cells, thereby possibly reducing the severity of leukemia.
However, prolonged exposure to IFN-γ can activate Treg cells and inhibitory immunological checkpoints, which can help leukemia evade immune surveillance and encounter an immunosuppressive environment.
Our review highlights IFN-γ's critical role in the complex interplay between the immune system and AML pathogenesis. Its dual role in both inhibiting and promoting leukemic processes has been highlighted.
However, future pre-clinical and clinical studies should focus on the specific mechanisms by which IFN-γ impacts AML progression and treatment outcomes, with the goal of achieving curative results for patients.
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