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

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 Cells, Lieping Chen

Research output: Contribution to journalArticlepeer-review

3235 Scopus citations


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-H1 tumors in vivo. These findings have implications for the design of T cell-based cancer immunotherapy.

Original languageEnglish (US)
Pages (from-to)793-800
Number of pages8
JournalNature Medicine
Issue number8
StatePublished - 2002
Externally publishedYes

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology
  • General Medicine


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