肿瘤细胞治疗研究
英文原题：From infection to immune exhaustion: The Epstein-Barr virus and its contribution to Immunosenescence.
EBV是一种常见的疱疹病毒，与慢性感染以及淋巴瘤、鼻咽癌等恶性肿瘤相关。
EBV是一种常见的疱疹病毒，与慢性感染及淋巴瘤、鼻咽癌等恶性肿瘤相关。EBV逃避免疫监视并诱导免疫功能障碍，对疾病进展至关重要。本综述探讨EBV如何驱动免疫耗竭和免疫衰老，重点关注其对T细胞和NK细胞的影响。慢性EBV感染引起持续性抗原刺激和免疫检查点分子（PD-1、LAG-3、TIM-3、CTLA-4）上调，导致T细胞和NK细胞增殖、细胞因子分泌及细胞毒性降低——这些是免疫耗竭的标志。EBV还调节细胞因子（IL-10、IL-18、IL-6、TNF-alpha），进一步破坏免疫监视并在肿瘤微环境中促进肿瘤生长。此外，EBV感染与耗竭免疫细胞群体（CD28- CD8+ T细胞和CD56 dim NK细胞）扩增相关，这些是免疫功能障碍和衰老的标志。免疫治疗，如检查点抑制剂，为逆转EBV诱导的免疫耗竭和恢复抗肿瘤免疫提供了希望。本综述强调EBV在免疫调节中的作用以及靶向EBV驱动免疫功能障碍的治疗潜力。
Epstein-Barr virus (EBV), a common herpesvirus, is linked to chronic infections and malignancies like lymphomas and nasopharyngeal carcinoma. EBV's evasion of immune surveillance and induction of immune dysfunction are critical for disease progression. This review explores how EBV drives immune exhaustion and immunosenescence, focusing on its effects on T and NK cells. Chronic EBV infection causes persistent antigenic stimulation and upregulation of immune checkpoint molecules (PD-1, LAG-3, TIM-3, CTLA-4), leading to reduced T and NK cell proliferation, cytokine secretion, and cytotoxicity-hallmarks of immune exhaustion. EBV also modulates cytokines (IL-10, IL-18, IL-6, TNF-alpha), further disrupting immune surveillance and promoting tumor growth within the tumor microenvironment. Furthermore, EBV infection is associated with expanded populations of exhausted immune cells (CD28- CD8+ T cells and CD56 dim NK cells), markers of immune dysfunction and aging. Immunotherapies, such as checkpoint inhibitors, offer promise for reversing EBV-induced immune exhaustion and restoring anti-tumor immunity. This review highlights EBV's role in immune regulation and the therapeutic potential of targeting EBV-driven immune dysfunction.
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