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DOI 10.1007/s00109-025-02553-w

Медицинская библиотека · Journal of molecular medicine (Berlin, Germany) · 2025

The role of innate immunity triggered by HPV infection in promoting cervical lesions.

Fu Kaiyu, Yang Xin, Zhang Mengpei, Yin Rutie

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Аннотация

Innate immunity is the immune system that organisms possess from birth. It is primarily responsible for the rapid, nonspecific recognition of pathogens when they invade, activating the host's immune response to eliminate. Cervical cancer is one of the most well-known tumors caused by human papillomavirus (HPV) infection. As the first line of defense against pathogens, innate immunity plays a crucial role in the response to HPV invasion, and there has been significant research in this area in recent years. The findings suggest that innate immune responses not only contribute to the clearance of HPV but may also facilitate the spread of the virus and the carcinogenic transformation of cervical epithelial cells. In this review, we comprehensively examine the activation of innate immune responses during HPV infection, the mechanisms by which HPV evades these immune defenses, and the role of innate immunity in promoting cervical intraepithelial neoplasia. Additionally, we explore the characteristics of innate immune responses within the tumor microenvironment of cervical cancer. Furthermore, we summarize recent advances in understanding the various mechanisms by which innate immune responses can be activated, with a focus on potential therapeutic implications. By reviewing the latest research, this article aims to provide valuable insights and stimulate further investigation into the role of innate immunity in HPV-associated cervical lesions, potentially leading to more effective strategies for prevention and treatment in the future.

Для цитирования: Fu Kaiyu, Yang Xin, Zhang Mengpei, Yin Rutie. The role of innate immunity triggered by HPV infection in promoting cervical lesions.. Journal of molecular medicine (Berlin, Germany). 2025. DOI: 10.1007/s00109-025-02553-w.

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