CTLA-4号机组
免疫原性
封锁
CD28
免疫学
免疫
调节器
免疫系统
癌症研究
T细胞
生物
抗体
医学
受体
内科学
生物化学
基因
作者
Dana R. Leach,Matthew F. Krummel,James P. Allison
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:1996-03-22
卷期号:271 (5256): 1734-1736
被引量:3536
标识
DOI:10.1126/science.271.5256.1734
摘要
One reason for the poor immunogenicity of many tumors may be that they cannot provide signals for CD28-mediated costimulation necessary to fully activate T cells. It has recently become apparent that CTLA-4, a second counterreceptor for the B7 family of costimulatory molecules, is a negative regulator of T cell activation. Here, in vivo administration of antibodies to CTLA-4 resulted in the rejection of tumors, including preestablished tumors. Furthermore, this rejection resulted in immunity to a secondary exposure to tumor cells. These results suggest that blockade of the inhibitory effects of CTLA-4 can allow for, and potentiate, effective immune responses against tumor cells.
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