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- Title
Tumor-associated B7-H1 promotes T-cell apoptosis: A potential mechanism of immune evasion.
- Authors
Dong, Haidong; Strome, Scott E.; Salomao, Diva R.; Tamura, Hideto; Hirano, Fumiya; Flies, Dallas B.; Roche, Patrick C.; Lu, Jun; Zhu, Gefeng; Tamada, Koji; Lennon, Vanda A.; Celis, Esteban; Chen, Lieping
- Abstract
B7-H1, a recently described member of the B7 family of costimulatory molecules, is thought to be involved in the regulation of cellular and humoral immune responses through the PD-1 receptor on activated T and B cells. We report here that, except for cells of the macrophage lineage, normal human tissues do not express B7-H1. In contrast, B7-H1 is abundant in human carcinomas of lung, ovary and colon and in melanomas. The pro-inflammatory cytokine interferon-γ upregulates B7-H1 on the surface of tumor cell lines. Cancer cell?associated B7-H1 increases apoptosis of antigen-specific human T-cell clones in vitro, and the apoptotic effect of B7-H1 is mediated largely by one or more receptors other than PD-1. In addition, expression of B7-H1 on mouse P815 tumor increases apoptosis of activated tumor-reactive T cells and promotes the growth of highly immunogenic B7-1+ tumors in vivo. These findings have implications for the design of T cell?based cancer immunotherapy.
- Subjects
T cells; APOPTOSIS; MONOCLONAL antibodies; CELL lines; BREAST cancer
- Publication
Nature Medicine, 2002, Vol 8, Issue 8, p793
- ISSN
1078-8956
- Publication type
Article
- DOI
10.1038/nm730