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Nat Med. 2002 Aug;8(8):793-800. Epub 2002 Jun 24.

Tumor-associated B7-H1 promotes T-cell apoptosis: a potential mechanism of immune evasion.

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  • 1Department of Immunology, Mayo Clinic, Rochester, Minnesota, USA.

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  • Nat Med 2002 Sep;8(9):1039.

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-gamma 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.

PMID:
12091876
[PubMed - indexed for MEDLINE]

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