The B7 family and cancer therapy: Costimulation and coinhibition
The B7 family and cancer therapy: Costimulation and coinhibition
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DOI：
10.1158/1078-0432.ccr-07-1030
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发表时间：
2007-09-15
影响因子：
11.5
通讯作者：
Allison, James P.
中科院分区：
文献类型：
--
作者：
Zang, Xingxing;Allison, James P.
获得性免疫反应的激活和发展是通过抗原肽-MHC复合体与T细胞抗原受体的结合而启动的。这种结合的结果由正负信号、共刺激和共抑制两种信号决定，主要由B7家族及其受体CD28家族之间的相互作用产生。共刺激和共抑制T细胞在控制免疫反应中的重要性被肿瘤作为免疫逃避途径加以利用。缺乏共刺激B7分子的表达使肿瘤对免疫系统不可见，而抑制性137分子的增强表达则保护它们免受有效的T细胞破坏。因此，对这些通路的调控对于发展有效的肿瘤免疫治疗至关重要。将我们关于共刺激和共抑制的基本知识转化为早期临床试验显示了相当大的希望。
The activation and development of an adaptive immune response is initiated by the engagement of a T-cell antigen receptor by an antigenic peptide-MHC complex. The outcome of this engagement is determined by both positive and negative signals, costimulation and coinhibition, generated mainly by the interaction between the B7 family and their receptor CD28 family. The importance of costimulation and coinhibition of T cells in controlling immune responses is exploited by tumors as immune evasion pathways. Absence of the expression of costimulatory B7 molecules renders tumors invisible to the immune system, whereas enhanced expression of inhibitory 137 molecules protects them from effective T cell destruction. Therefore, the manipulation of these pathways is crucial for developing effective tumor immunotherapy. Translation of our basic knowledge of costimulation and coinhibition into early clinical trials has shown considerable promise.