二酰甘油激酶
癌症研究
细胞毒性T细胞
免疫疗法
激酶
癌症
癌症免疫疗法
T细胞
免疫系统
癌细胞
下调和上调
生物
限制
免疫学
医学
细胞生物学
蛋白激酶C
体外
遗传学
基因
工程类
机械工程
作者
Javier Arranz-Nicolás,Isabel Mérida
出处
期刊:Advances in biological regulation
日期:2020-01-01
卷期号:75: 100663-100663
被引量:12
标识
DOI:10.1016/j.jbior.2019.100663
摘要
In the recent years, the arsenal of anti-cancer therapies has evolved to target T lymphocytes and restore their capacity to destroy tumor cells. However, the clinical success is limited, with a large number of patients that never responds and others that ultimately develop resistances. Overcoming the hypofunctional state imposed by solid tumors to T cells has revealed critical but challenging due to the complex strategies that tumors employ to evade the immune system. The Diacylglycerol kinases (DGK) limit DAG-dependent functions in T lymphocytes and their upregulation in tumor-infiltrating T lymphocytes contribute to limit T cell cytotoxic potential. DGK blockade could reinstate T cell attack on tumors, limiting at the same time tumor cell growth, thanks to the DGK positive input into several oncogenic pathways. In this review we summarize the latest findings regarding the regulation of specific DGK isoforms in healthy and anergic T lymphocytes, as well as their contribution to oncogenic phenotypes. We will also revise the latest advances in the search for pharmacological inhibitors and their potential as anti-cancer agents, either alone or in combination with immunomodulatory agents.
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