| Literature DB >> 19875977 |
Seunggu J Han1, Brian J Ahn, James S Waldron, Isaac Yang, Shanna Fang, Courtney A Crane, Russell O Pieper, Andrew T Parsa.
Abstract
B7 homolog 1 (B7-H1) is a recently discovered immunoresistance protein that is regulated posttranscriptionally after PTEN loss in malignant glioma, a deadly form of brain tumor. Here, the impact of gamma-interferon-mediated activation of B7-H1 was investigated in glioblastoma patients with PTEN loss. Lymphocytes and T cells were selected for apoptosis assays after 1 : 1 coculture with autologous glioma cells. Gamma interferon treatment of PTEN-deficient tumors resulted in superinduction of B7-H1 protein that correlated with increased T-cell apoptosis, an effect dependent upon activation of the PI3-kinase pathway. The combination of PTEN loss and gamma-interferon exposure in glioblastoma patients results in an exceptionally immunoresistant phenotype that may negate adaptive immunity through induction of T-cell apoptosis.Entities:
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Year: 2009 PMID: 19875977 PMCID: PMC3666317 DOI: 10.1097/WNR.0b013e32833188f7
Source DB: PubMed Journal: Neuroreport ISSN: 0959-4965 Impact factor: 1.837