免疫系统
癌症研究
免疫监视
癌变
免疫疗法
肿瘤坏死因子α
肿瘤微环境
生物
癌症
免疫学
癌症免疫疗法
免疫检查点
肿瘤进展
遗传学
作者
Alaleh Mohammadi,Souzan Najafi,Mohammad Amini,Behzad Mansoori,Amir Baghbanzadeh,Jörg D. Hoheisel,Behzad Baradaran
出处
期刊:Life Sciences
[Elsevier]
日期:2022-09-01
卷期号:304: 120709-120709
被引量:7
标识
DOI:10.1016/j.lfs.2022.120709
摘要
Immune checkpoints are vital molecules that regulate T-cell function by activation or inhibition. Among the immune checkpoint molecules, the B7-family proteins are significantly involved in the immune escape of tumor cells. By binding to inhibitory receptors, they can suppress T-cell-mediated immunity. B7-family proteins are found at various stages of tumor microenvironment formation and promote tumorigenesis and tumor progression. B7-H6 (encoded by gene NCR3LG1) is a prominent member of the family. It has unique immunogenic properties and is involved in natural killer (NK) cell immunosurveillance by binding to the NKp30 receptor. High B7-H6 expression in certain tumor types and shortage of or low expression in healthy cells - except in cases of inflammatory or microbial stimulation - have made the protein an attractive target of research activities in recent years. The avoidance of NK-mediated B7-H6 detection is a mechanism through which tumor cells escape immune surveillance. The stimulation of tumorigenesis occurs by suppressing caspase cascade initiation and anti-apoptosis activity stimulation via the STAT3 pathway. The B7-H6-NKp30 complex on the tumor membrane activates the NK cells and releases both tumor necrosis factor alpha (TNF-α) and interferon gamma (IFN-γ). B7-H6 is highly expressed in a wide range of tumor cells, including glioma, hematologic malignant tumors, and breast cancer cells. Clinical examination of cancer patients indicated that the expression of B7-H6 is related to distant metastasis status and permits postoperative prognosis. Because of its unique properties, B7-H6 has a high potential be utilized as a biological marker for cancer diagnosis and prognosis, as well as a target for novel treatment options.
科研通智能强力驱动
Strongly Powered by AbleSci AI