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J Mol Med (Berl). 2003 May;81(5):281-7. Epub 2003 Apr 30.

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

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1
Department of Immunology, Mayo Medical and Graduate Schools, Mayo Clinic, 200 First Street Southwest, Rochester, MN 55905, USA.

Abstract

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.

PMID:
12721664
DOI:
10.1007/s00109-003-0430-2
[Indexed for MEDLINE]
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