Chen Zeping, Zhao Binzhu
Department of Gynecology, Chengdu Pidu District Hospital of Traditional Chinese Medicine, Chengdu, China.
Front Immunol. 2025 Apr 8;16:1586806. doi: 10.3389/fimmu.2025.1586806. eCollection 2025.
Human papillomavirus (HPV), a double-stranded DNA virus linked to various malignancies, poses a significant global public health challenge. In cervical cancer, persistent infection with high-risk HPV genotypes, particularly HPV-16 and HPV-18, initiates immune evasion mechanisms within the tumor microenvironment. The polarization of tumor-associated macrophages (TAMs) from M1 to M2 phenotypes promotes cervical carcinogenesis, metastasis, and therapeutic resistance via establishing an immunosuppressive microenvironment. This review provides a comprehensive overview of HPV-induced immune evasion pathways, including MHC downregulation, T-cell impairment, regulatory T cell induction, and cGAS-STING pathway inhibition. Furthermore, describe the pivotal role of TAMs in cervical cancer progression, focusing on their phenotypic plasticity, pro-tumoral functions, and potential as therapeutic targets. By elucidating these cellular and molecular dynamics, this review aims to support advanced research. Targeting TAM polarization through immunotherapies and nanomedicine-based strategies represents a promising strategy for enhancing patient outcomes.
人乳头瘤病毒（HPV）是一种与多种恶性肿瘤相关的双链DNA病毒，对全球公共卫生构成重大挑战。在宫颈癌中，高危HPV基因型的持续感染，尤其是HPV-16和HPV-18，会在肿瘤微环境中启动免疫逃逸机制。肿瘤相关巨噬细胞（TAM）从M1表型向M2表型的极化通过建立免疫抑制微环境促进宫颈癌的发生、转移和治疗抵抗。本综述全面概述了HPV诱导的免疫逃逸途径，包括MHC下调、T细胞损伤、调节性T细胞诱导和cGAS-STING途径抑制。此外，描述了TAM在宫颈癌进展中的关键作用，重点关注其表型可塑性、促肿瘤功能以及作为治疗靶点的潜力。通过阐明这些细胞和分子动力学，本综述旨在支持深入研究。通过免疫疗法和基于纳米医学的策略靶向TAM极化是改善患者预后的一种有前景的策略。
