免疫监视
免疫编辑
免疫系统
医学
免疫疗法
肥胖
癌症
免疫学
癌症免疫疗法
内科学
癌症研究
肿瘤科
生物信息学
生物
作者
Alexander Piening,Ellen C. Ebert,Carter Gottlieb,Niloufar Khojandi,Lindsey M. Kuehm,Stella G. Hoft,Kelly D. Pyles,Kyle S. McCommis,Richard J. DiPaolo,Stephen T. Ferris,Elise Alspach,Ryan M. Teague
标识
DOI:10.1038/s41467-024-47359-5
摘要
Abstract Obesity is a well-established risk factor for human cancer, yet the underlying mechanisms remain elusive. Immune dysfunction is commonly associated with obesity but whether compromised immune surveillance contributes to cancer susceptibility in individuals with obesity is unclear. Here we use a mouse model of diet-induced obesity to investigate tumor-infiltrating CD8 + T cell responses in lean, obese, and previously obese hosts that lost weight through either dietary restriction or treatment with semaglutide. While both strategies reduce body mass, only dietary intervention restores T cell function and improves responses to immunotherapy. In mice exposed to a chemical carcinogen, obesity-related immune dysfunction leads to higher incidence of sarcoma development. However, impaired immunoediting in the obese environment enhances tumor immunogenicity, making the malignancies highly sensitive to immunotherapy. These findings offer insight into the complex interplay between obesity, immunity and cancer, and provide explanation for the obesity paradox observed in clinical immunotherapy settings.
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