| Literature DB >> 22138406 |
Xavier Frigola, Brant A Inman, Christopher J Krco, Xin Liu, Susan M Harrington, Peggy A Bulur, Allan B Dietz, Haidong Dong, Eugene D Kwon.
Abstract
Tumor cells aberrantly express several T cell inhibitory molecules including members of the B7-H co-regulatory family. Presumably tumor-expressed B7-H1 and B7-H3 confer resistance to elimination by the immune system. In addition, elevated levels of soluble B7-H1 (sB7-H1) has been identified in the sera of cancer patients, including renal carcinoma patients and is associated with increased cancer related death. Here we report that sB7-H1 is produced and released by activated mature dendritic cells (mDC). Immature DC, macrophages, monocytes, or T cells are refractory to releasing sB7-H1. Exposure of CD4+ and CD8+ T cells to mDC-derived sB7-H1 molecules induced apoptosis. These data suggest that the immunobiology of B7-H1 is perhaps more complex than previously thought. sB7-H1 molecules may represent an unanticipated contributing factor to immune homeostasis. That both immune and tumor cells can be sources of sB7-H1 suggests that optimization of co-regulatory blockade immunotherapy for solid malignancies of necessity will require impact of targeting tumor and immune-derived B7-H1 molecules.Entities:
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Year: 2011 PMID： 22138406 PMCID： PMC3901160 DOI： 10.1016/j.imlet.2011.11.001
Source DB: PubMed Journal: Immunol Lett ISSN： 0165-2478 Impact factor: 3.685