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
Whether PCD yields effective immune activation therefore depends on its capacity to induce antigen release and presentation as well as on the death mode itself.Distinct forms of PCD can promote antigen presentation and adaptive immune activation by inducing ICD.；ICD-associated antigen presentation can drive DC maturation and T cell activation, but how different death modes regulate antigen-presentation networks in OPSCC remains unclear.；Moreover, mitochondrial targeting overcomes chemoresistance via coactivation of apoptosis and ferroptosis in doxorubicin-resistant breast cancer models (Hao et al., 2025); however, the relevance of these mechanisms to OPSCC remains unknown.
方法
Despite continuing advances in therapies such as immune checkpoint inhibitors (ICIs), some patients do not achieve durable clinical benefit because of heterogeneity in the TIME, immune evasion and treatment resistance (Liu X. et al., 2022; Noji et al., 2022).；PCD, as a key link between tumour-cell fate and immune regulation, can affect treatment outcome by altering the immunological consequences of cell death.；Compared with HPV-positive HNSCC cohorts and with normal or inflamed tonsils, HPV-negative HNSCC contains a substantially higher proportion of Tregs without a significant change in CD8+ T cell frequency, suggesting that viral status shapes distinct TIME states by selectively altering immune-cell composition (Ruffin et al., 2021).Beyond the accumulation of immunosuppressive cells, altered effector-cell function contributes to immune dysregulation in OPC.
核心结论
Immune-cell composition, immune-checkpoint signalling and tumour-antigen recognition within the TIME collectively shape treatment response (Tosi et al., 2022).；HPV-positive tumours occupy multiple immune states and show greater niche diversity, demonstrating that HPV infection alone does not impose a fixed immune phenotype (Kim et al., 2020; An et al., 2026).Single-cell analyses further reveal a more active network of immune-cell interactions in HPV-positive OPC.；In a metformin clinical trial, the enhancement in tumor cell apoptosis was markedly greater in HPV-negative HNSCC than in HPV-positive OPSCC, whereas nodal specimens from patients who received metformin demonstrated increased CD8+ effector T-cell and FoxP3+ regulatory T-cell infiltration (Curry et al., 2018).Dysregulated apoptotic pathways also sustain tumour stemness and alter tumour-cell clearance under therapeutic pressure.
局限
However, how distinct PCD modes cooperate to regulate immune evasion, antitumour immune activation and treatment response in OPC remains poorly resolved, as does the mechanistic link between PCD-dependent immune regulation and clinical benefit.This Review encapsulates signaling mechanisms of different PCD modes that regulate immunity in OPC.；Persistent antigenic stimulation, immune-checkpoint activation and local regulatory signals can, however, promote exhausted CD8+ T-cell states characterized by increased inhibitory-receptor expression and heterogeneous effector function, thereby constraining durable antitumour immunity (Qiu et al., 2023; Rao et al., 2024).CD8+ T cell exhaustion is one of the major features of immune dysfunction in OPC.；In the absence of specific functional T cell populations, however, PD-1 blockade does not reverse the severe dysfunction of CD8+ TEx-EEx tumour-infiltrating lymphocytes (TILs) in the TIME of non-responding patients with locally advanced HNSCC, further identifying effector-cell state as a major constraint on immunotherapy response (Oliveira et al., 2023).HPV status further shapes the composition and function of effector immune cells in OPC.
对本项目的价值
中高价值：属「营养感知—自噬—蛋白稳态轴」方向；mTOR / 自噬 / 蛋白质稳态栏目可用作本项目文献库与综述素材。 ｜ 价值分 3.4/5（★★★☆☆）
全文来源
PubMed PMC JATS（正文 106,335 字符，题名指纹 0.77，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：程序性细胞死亡介导口咽癌免疫逃逸与抗肿瘤免疫的机制
- 英文标题：Mechanisms by which programmed cell death mediates immune evasion and antitumour immunity in oropharyngeal cancer.
- 期刊与标识：Frontiers in cell and developmental biology · PMID 42978979 · DOI 10.3389/fcell.2026.1966827 · PMC PMC13728170