Integrated Immune Escape in Cervical Cancer: HLA-I Dysfunction and Immune Checkpoint Signaling

Persistent infection with high-risk human papillomavirus (hrHPV) is the principal cause of cervical cancer and initiates a complex process of immune evasion that enables malignant progression despite continuous expression of the viral oncoproteins E6 and E7. Effective antitumor immunity depends on coordinated antigen presentation through human leukocyte antigen class I (HLA-I) molecules, activation of CD8+ cytotoxic T lymphocytes, and balanced regulation of immune responses. During cervical carcinogenesis, these mechanisms are progressively disrupted through HLA-I downregulation, CD8+ T-cell exhaustion, expansion of FOXP3+ regulatory T cells, and activation of the PD-1/PD-L1 and CTLA-4 immune checkpoint pathways, ultimately establishing an immunosuppressive tumor microenvironment that promotes immune escape. This narrative review integrates current evidence on HLA-I-mediated antigen presentation, CD8+ cytotoxic T-cell function, FOXP3+ regulatory T cells, and immune checkpoint signaling into a unified model of immune escape during cervical carcinogenesis. In addition, it discusses the clinical implications of these interconnected mechanisms, including immune checkpoint inhibition, emerging therapeutic strategies, integrated immune profiling, and future directions in personalized immunotherapy. A comprehensive understanding of the interactions between antigen presentation, immune-cell function, and immune checkpoint regulation provides the biological foundation for current and future immunotherapeutic approaches. Integrating molecular, cellular, and spatial immune characteristics may improve patient stratification, optimize treatment selection, and facilitate the implementation of precision immuno-oncology in cervical cancer.