Tumor-associated B7-H1 promotes T-cell apoptosis: A potential mechanism of immune evasion View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2002-06-24

AUTHORS

Haidong Dong, Scott E. Strome, Diva R. Salomao, Hideto Tamura, Fumiya Hirano, Dallas B. Flies, Patrick C. Roche, Jun Lu, Gefeng Zhu, Koji Tamada, Vanda A. Lennon, Esteban Celis, Lieping Chen

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. More... »

PAGES

793-800

Journal

TITLE

Nature Medicine

ISSUE

8

VOLUME

8

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nm730

    DOI

    http://dx.doi.org/10.1038/nm730

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1043110107

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/12091876


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