BTLA公司
癌症研究
细胞生物学
生物
T细胞
癌症免疫疗法
肿瘤微环境
免疫系统
免疫疗法
化学
免疫学
作者
Tian-You Cheng,Ya-Juan Liu,Hong Yan,Yi-Bo Xi,Li-Qiang Duan,Yang Wang,Tian-Tian Zhang,Yin-Min Gu,Xiao-Dong Wang,Chang-Xin Wu,Shan Gao
出处
期刊:Cells
[MDPI AG]
日期:2022-12-12
卷期号:11 (24): 4021-4021
被引量:2
标识
DOI:10.3390/cells11244021
摘要
B and T lymphocyte attenuator (BTLA) is an immune checkpoint molecule that mediates the escape of tumor cells from immunosurveillance. Consequently, BTLA and its ligand herpesvirus entry mediator (HVEM) are potentially immunotherapeutic targets. However, the potential effects of BTLA on tumor cells remain incompletely unknown. Here, we show that BTLA is expressed across a broad range of tumor cells. The depletion of BTLA or HVEM promotes cell proliferation and colony formation, which is reversed by the overexpression of BTLA in BTLA knockout cells. In contrast, overexpression of BTLA or HVEM inhibits tumor cell proliferation and colony formation. Furthermore, the proliferation of a subpopulation with high BTLA was also significantly slower than that of the low BTLA subpopulation. Mechanistically, the coordination of BTLA and HVEM inhibits its major downstream extracellular regulated protein kinase (ERK1/2) signaling pathway, thus preventing tumor cell growth. This study demonstrates that tumor cell-intrinsic BTLA/HVEM is a potential tumor suppressor and is likely to have a potential antagonist for immunotherapy, thus representing a potential biomarker for the optimal cancer immunotherapeutic treatment.
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