Ebrahimi Fatemeh, Rasizadeh Reyhaneh, Jafari Sajjad, Baghi Hossein Bannazadeh
Immunology Research Centre, Tabriz University of Medical Sciences, Tabriz, Iran.
Department of Virology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Infect Agent Cancer. 2024 Dec 18;19(1):63. doi: 10.1186/s13027-024-00624-0.
Anal cancer incidence is rising globally, driven primarily by human papillomavirus (HPV) infection. HPV, especially high-risk types 16 and 18, is considered a necessary cause of anal squamous cell carcinoma. Certain populations like people living with HIV, men who have sex with men, inflammatory bowel disease patients, smokers, and those with compromised immunity face elevated risk. Chronic inflammation facilitates viral persistence, cell transformation, and immune evasion through pathways involving the PD-1/PD-L1 axis. HIV coinfection further increases risk by impairing immune surveillance and epithelial integrity while promoting HPV oncogene expression. Understanding these inflammatory processes, including roles of CD8 + T cells and PD-1/PD-L1, could guide development of immunotherapies against anal cancer. This review summarizes current knowledge on inflammation's role in anal cancer pathogenesis and the interplay between HPV, HIV, and host immune factors.
全球范围内，肛管癌的发病率正在上升，主要是由人乳头瘤病毒（HPV）感染驱动的。HPV，尤其是高危型16和18型，被认为是肛管鳞状细胞癌的必要病因。某些人群，如艾滋病毒感染者、男男性行为者、炎症性肠病患者、吸烟者以及免疫力受损者，面临着更高的风险。慢性炎症通过涉及PD-1/PD-L1轴的途径促进病毒持续存在、细胞转化和免疫逃逸。HIV合并感染通过损害免疫监视和上皮完整性，同时促进HPV癌基因表达，进一步增加风险。了解这些炎症过程，包括CD8 + T细胞和PD-1/PD-L1的作用，可为肛管癌免疫疗法的开发提供指导。本综述总结了目前关于炎症在肛管癌发病机制中的作用以及HPV、HIV和宿主免疫因素之间相互作用的知识。
