Your browser doesn't support javascript.
loading
Gamma interferon-mediated superinduction of B7-H1 in PTEN-deficient glioblastoma: a paradoxical mechanism of immune evasion.
Han, Seunggu J; Ahn, Brian J; Waldron, James S; Yang, Isaac; Fang, Shanna; Crane, Courtney A; Pieper, Russell O; Parsa, Andrew T.
Afiliación
  • Han SJ; Department of Neurological Surgery, University of California at San Francisco, San Francisco, California 94117, USA.
Neuroreport ; 20(18): 1597-602, 2009 Dec 09.
Article en En | MEDLINE | ID: mdl-19875977
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.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias Encefálicas / Antígenos CD / Interferón gamma / Glioblastoma / Fosfohidrolasa PTEN / Antineoplásicos Límite: Humans Idioma: En Revista: Neuroreport Asunto de la revista: NEUROLOGIA Año: 2009 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias Encefálicas / Antígenos CD / Interferón gamma / Glioblastoma / Fosfohidrolasa PTEN / Antineoplásicos Límite: Humans Idioma: En Revista: Neuroreport Asunto de la revista: NEUROLOGIA Año: 2009 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido