B7-H1 pathway and its role in the evasion of tumor immunity

Haidong Dong, Lieping Chen

Research output: Contribution to journalReview articlepeer-review

235 Scopus citations


B7-H1 is a recently identified member of the B7 family molecules. Upon ligation to its receptors on T cells it regulates activation and differentiation of T cells. B7-H1 preferentially costimulates IL-10 production in resting T cells and further induces the apoptosis of activated T cells. PD-1 is a receptor of B7-H1 and is shown to mediate the inhibition of activated T cell response, presumably by inhibiting cell cycle progression. The expression of B7-H1 protein is limited to macrophage lineage of cells in normal tissues, although its mRNA transcription is found in a broad range of tissues. In contrast, B7-H1 is abundant in various human cancers. The tumor-associated B7-H1 increases apoptosis of antigen specific T cells, leading to growth of immunogenic tumor growth in vivo. Current data suggest that B7-H1 regulates the organ-specific tolerance in normal tissue and may contribute to immune evasion by cancers. Selective manipulation of B7-H1 pathway thus aids in the design of new regimens in the treatment of human autoimmune disease and the control of malignant cancers.

Original languageEnglish (US)
Pages (from-to)281-287
Number of pages7
JournalJournal of Molecular Medicine
Issue number5
StatePublished - May 1 2003


  • Immunosuppression
  • T cell activation
  • Tumor

ASJC Scopus subject areas

  • Molecular Medicine
  • Drug Discovery
  • Genetics(clinical)


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