时间标签：数据日期 2026-11-03 · 生成时间 2026-11-03 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/10/31 – 2026/11/03 ｜ 情报发生日期 2026-11-03
研究问题
Whether such strategies work in humans is unclear, but the circuit model offers a clear rationale for testing them.；Although DDR signaling has been linked to PD-L1 expression in cell-based models, whether it precedes PD-L1 upregulation in aging tissues, or whether other senescence-associated signals act independently of DDR, is not yet clear.；Third, the relative contribution of transcriptional and post-translational mechanisms to PD-L1 upregulation likely varies across tissues. p16-mediated stabilization has been demonstrated in alveolar macrophages and epithelial cells ( Majewska et al., 2024 ), but whether this mechanism operates with similar efficiency in other cell types remains unclear ( Salminen, 2024 ).
方法
（原文未给出可直接抽取的对应表述）
核心结论
These data indicate that PD-L1 is not merely a senescence marker but a functionally relevant checkpoint that protects senescent cells from immune elimination.
局限
First, the causal relationship between DDR signaling and PD-L1 upregulation in vivo remains to be fully defined.
对本项目的价值
中高价值：属「衰老细胞清除 / SASP 轴」方向；细胞衰老 / senolytics / SASP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 19,301 字符，题名指纹 0.90，已过 DOI 逐字 + 题名指纹 + 正文长度三重归属校验）
原文题录
- 中文题名：DNA 损伤应答驱动衰老细胞 PD-L1 表达：免疫逃逸与免疫衰老的含义
- 英文标题：DNA damage response as a driver of PD-L1 expression in cellular senescence: implications for immune evasion and immunosenescence.
- 期刊与标识：Front Cell Dev Biol · PMID 42964463 · DOI 10.3389/fcell.2026.1974523 · PMC PMC13719894 · EDAT 2026-10-31