Gamma interferon-mediated superinduction of B7-H1 in PTEN-deficient glioblastoma: A paradoxical mechanism of immune evasion

Seunggu J. Han, Brian J. Ahn, James S. Waldron, Isaac Yang, Shanna Fang, Courtney A. Crane, Russell O. Pieper, Andrew T. Parsa

Research output: Contribution to journalArticle

25 Scopus citations


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 γ-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 γ-interferon exposure in glioblastoma patients results in an exceptionally immunoresistant phenotype that may negate adaptive immunity through induction of T-cell apoptosis.

Original languageEnglish (US)
Pages (from-to)1597-1602
Number of pages6
Issue number18
StatePublished - Dec 1 2009



  • B7 homolog 1
  • Glioma
  • Immune evasion
  • Immunoresistance
  • Interferon gamma
  • Programmed death ligand-1

ASJC Scopus subject areas

  • Neuroscience(all)

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