免疫系统
肿瘤微环境
癌症
癌症研究
信号转导
免疫疗法
胰岛素
炎症
细胞因子
癌细胞
癌症免疫疗法
生物
免疫学
医学
内分泌学
内科学
细胞生物学
作者
Veronica Vella,Ernestina Marianna De Francesco,Eduardo Bonavita,Rosamaria Lappano,Antonino Belfiore
标识
DOI:10.1016/j.tem.2022.04.009
摘要
Type I interferons (IFN-Is) are prototypical inflammatory cytokines produced in response to stress. IFN-Is have a critical role in antitumor immunity by driving the activation of leukocytes and favoring the elimination of malignant cells. However, IFN-I signaling in cancer, specifically in the tumor microenvironment (TME), can have opposing roles. Sustained IFN-I stimulation can promote immune exhaustion or enable tumor cell-intrinsic malignant features. Herein, we discuss the potential impact of the insulin/insulin-like growth factor system (I/IGFs) and of metabolic disorders in aberrant IFN-I signaling in cancer. We consider the possibility that targeting I/IGFs, especially in patients with cancer affected by metabolic disorders, contributes to an effective strategy to inhibit deleterious IFN-I signaling, thereby restoring sensitivity to various cancer therapies, including immunotherapy.
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