生物
免疫系统
干扰素
免疫疗法
细胞生物学
CD8型
信号转导
细胞毒性T细胞
受体
抗原
免疫学
癌症研究
生物化学
体外
作者
Sandra Hervás-Stubbs,José Luis Perez-Gracia,Ana Rouzaut,Miguel F. Sanmamed,Agnès Le Bon,Ignacio Melero
标识
DOI:10.1158/1078-0432.ccr-10-1114
摘要
Type I interferons (IFN-I) are well-known inducers of tumor cell apoptosis and antiangiogenesis via signaling through a common receptor interferon alpha receptor (IFNAR). IFNAR induces the Janus activated kinase-signal transducer and activation of transcription (JAK-STAT) pathway in most cells, along with other biochemical pathways that may differentially operate, depending on the responding cell subset, and jointly control a large collection of genes. IFNs-I were found to systemically activate natural killer (NK) cell activity. Recently, mouse experiments have shown that IFNs-I directly activate other cells of the immune system, such as antigen-presenting dendritic cells (DC) and CD4 and CD8 T cells. Signaling through the IFNAR in T cells is critical for the acquisition of effector functions. Cross-talk between IFNAR and the pathways turned on by other surface lymphocyte receptors has been described. Importantly, IFNs-I also increase antigen presentation of the tumor cells to be recognized by T lymphocytes. These IFN-driven immunostimulatory pathways offer opportunities to devise combinatorial immunotherapy strategies.
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