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On March 14, 2026, the team led by Professor Jin Tengchuan from the Life Sciences and Medicine Department and the National Key Laboratory of Immune Response and Immunotherapy at the University of Science and Technology of China published a review article titled "The T-Cell Response Mechanism in Human Papillomavirus-Associated Cervical Cancer and New Strategies for Immunotherapy" in iNew Medicine. This review systematically analyzed the core mechanism of T-cell immune response in HPV-associated cervical cancer and comprehensively summarized the cutting-edge strategies of T-cell-based immunotherapy, bringing a new theoretical perspective and clinical transformation ideas to the fight against this highly prevalent tumor among women.
The global burden of cervical cancer is extremely severe. According to data statistics in 2022, there were approximately 660,000 new cases of cervical cancer worldwide each year. In China, the incidence of this disease is still increasing year by year. As early as 2008, German scientist Harald zur Hausen won the Nobel Prize in Physiology or Medicine for discovering the association between HPV infection and cervical cancer. Current research has confirmed that 96% to 99.7% of cervical cancer cases are related to HPV infection, and among them, HPV types 16 and 18, the two high-risk types, account for approximately 70% of global cervical cancer cases.
HPV is a double-stranded DNA virus that mainly infects human skin and mucosal tissues. More than 200 subtypes have been discovered, and the International Committee on Taxonomy of Viruses has classified them into 5 genera based on differences in their L1 sequences. The α genus contains the most relevant high-risk subtypes to human diseases (Figure 1). Clinically, HPV is classified into high-risk and low-risk types based on its carcinogenic potential. The two cancer proteins encoded by its genome, E6 and E7, are the core drivers of cell malignant transformation - E6 protein targets and degrades the tumor suppressor gene p53, preventing damaged cells from completing DNA repair or initiating apoptosis, while E7 protein inactivates the retinoblastoma protein pRB, leading to uncontrolled cell cycle and abnormal proliferation. The combined action not only disrupts normal cell regulation but also continuously induces genomic instability, promoting the progression of cervical epithelial cells from precancerous lesions to invasive cancer (Figure 2). Notably, the vast majority of HPV infections are cleared by the human immune system within several years, and only a few persistent infections will eventually develop into cancer, which also means that host immune function, especially T-cell-mediated adaptive immunity, is the core factor determining the outcome of HPV infection, laying a crucial theoretical foundation for cervical cancer immunotherapy.
