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

doi:10.1097/WNR.0b013e32833188f7

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 journal › Article › peer-review

35 Scopus citations

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 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 language	English (US)
Pages (from-to)	1597-1602
Number of pages	6
Journal	NeuroReport
Volume	20
Issue number	18
DOIs	https://doi.org/10.1097/WNR.0b013e32833188f7
State	Published - Dec 2009
Externally published	Yes

Keywords

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

ASJC Scopus subject areas

General Neuroscience

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10.1097/WNR.0b013e32833188f7

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

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 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.",

keywords = "B7 homolog 1, Glioma, Immune evasion, Immunoresistance, Interferon gamma, Programmed death ligand-1",

author = "Han, {Seunggu J.} and Ahn, {Brian J.} and Waldron, {James S.} and Isaac Yang and Shanna Fang and Crane, {Courtney A.} and Pieper, {Russell O.} and Parsa, {Andrew T.}",

year = "2009",

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doi = "10.1097/WNR.0b013e32833188f7",

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T2 - A paradoxical mechanism of immune evasion

AU - Han, Seunggu J.

AU - Ahn, Brian J.

AU - Waldron, James S.

AU - Yang, Isaac

AU - Fang, Shanna

AU - Crane, Courtney A.

AU - Pieper, Russell O.

AU - Parsa, Andrew T.

PY - 2009/12

Y1 - 2009/12

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AB - 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.

KW - B7 homolog 1

KW - Glioma

KW - Immune evasion

KW - Immunoresistance

KW - Interferon gamma

KW - Programmed death ligand-1

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

Abstract

Keywords

ASJC Scopus subject areas

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