| pubmed-article:17683946 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17683946 | lifeskim:mentions | umls-concept:C0020964 | lld:lifeskim |
| pubmed-article:17683946 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:17683946 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:17683946 | pubmed:dateCreated | 2007-8-13 | lld:pubmed |
| pubmed-article:17683946 | pubmed:abstractText | Costimulation was originally shown to be important in T-cell activation and effector differentiation. Recent characterization of B7/butyrophilin and members of the CD28 superfamily has revealed a large number of negative costimulatory molecules that dampen T-cell activation and regulate immune tolerance. Some of these molecules have been shown to be upregulated in the tumor microenvironment and may serve as potential targets for augmenting anti-tumor immunity. In this article, we summarize recent developments in the field of inhibitory costimulation and discuss the future direction of therapeutic manipulation of inhibitory costimulation in tumor immunotherapy. | lld:pubmed |
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