时间标签：数据日期 2026-11-05 · 生成时间 2026-11-05 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/11/02 – 2026/11/06 ｜ 情报发生日期 2026-11-05
研究问题
However, whether NAT10 plays a role in regulating Tregs in the context of antitumor immunity remains largely unknown.In this study, we demonstrate that NAT10 supported Treg infiltration and activation within the TME.；Given that TI Tregs may arise from CD4+ T cells activated by antigen presentation via MHC molecules on dendritic or tumor cells, we examined whether Nat10 expression in TI Tregs, or MHC molecule expression in antigen-presenting cells, was induced during anti–PD-1, cisplatin, or paclitaxel therapy (Supplemental Figure 4A).；To investigate whether Nat10 ablation destabilizes intratumoral Tregs, we generated Foxp3GFP-cre-ERT2 × Nat10fl/fl mice in which tamoxifen administration triggers FOXP3+ Treg-specific deletion of Nat10 and simultaneous GFP expression.
方法
IntroductionIncreasing evidence indicates that elevated frequencies of tumor-infiltrating (TI) Tregs correlate with poor prognosis in patients with cancer.；Among these, N-acetyltransferase 10 (NAT10), the first characterized enzyme catalyzing N4-acetylcytidine (ac4C) mRNA modifications, has been shown to regulate T cell proliferation and antiviral responses (28) and is involved in cycling T cell–driven autoimmunity in mice (29).；However, whether NAT10 plays a role in regulating Tregs in the context of antitumor immunity remains largely unknown.In this study, we demonstrate that NAT10 supported Treg infiltration and activation within the TME.
核心结论
IntroductionIncreasing evidence indicates that elevated frequencies of tumor-infiltrating (TI) Tregs correlate with poor prognosis in patients with cancer.；Notably, functionally heterogeneous Treg subpopulations contribute to early lung tumorigenesis, metastasis, and immunotherapy resistance (13–15).Given these findings, TI Tregs are considered a major barrier to effective immunotherapy.；However, whether NAT10 plays a role in regulating Tregs in the context of antitumor immunity remains largely unknown.In this study, we demonstrate that NAT10 supported Treg infiltration and activation within the TME.
局限
Tregs, a subset of CD4+ T cells defined by the expression of the transcription factor FOXP3, are crucial for maintaining immune homeostasis and preventing autoimmunity (1–4); however, they also suppress antitumor immunity and hinder cancer immunotherapy (5–7).；However, systemic Treg depletion carries a high risk of autoimmunity and inflammation, underscoring the need for strategies that selectively target TI Tregs (8).；Therefore, understanding the mechanisms governing TI Treg accumulation and suppressive function is essential for improving immunotherapy outcomes.FOXP3 is indispensable for Treg identity and suppressive function; however, its expression alone does not ensure full lineage commitment or functional maturation, especially under tumor-associated stress (13).
对本项目的价值
中高价值：属「干细胞 / 部分重编程与再生」方向；干细胞 / 再生 / 重编程栏目可用作本项目文献库与综述素材。 ｜ 价值分 3.0/5（★★★☆☆）
全文来源
PubMed PMC JATS（正文 46,554 字符，题名指纹 0.83，已过 PubMed PMCID 官方关联 + 题名指纹 + 正文长度归属校验）
原文题录
- 中文题名：靶向 N-乙酰转移酶 10 重编程 Treg 功能以增强小鼠肺肿瘤抗 PD-1 免疫治疗敏感性
- 英文标题：Targeting N-acetyltransferase 10 reprograms Treg function to enhance anti-PD-1 immunotherapy sensitivity in murine lung tumors.
- 期刊与标识：The Journal of clinical investigation · PMID 42969236 · DOI 10.1172/JCI189034 · PMC PMC13722382