Expression of the B7-Related Molecule B7-H1 by Glioma Cells

A Potential Mechanism of Immune Paralysis

Sabine Wintterle, Bettina Schreiner, Meike Mitsdoerffer, Dagmar Schneider, Lieping Chen, Richard Meyermann, Michael Weller, Heinz Wiendl

Research output: Contribution to journalArticle

Abstract

Human glioblastoma is a highly lethal tumor that is known for its immune inhibitory capabilities B7-homologue 1 (B7-H1), a recently identired homologue of B71/2 (CD80/86), has been described to exert costimulatory and immune regulatory functions We investigated the expression and the functional activity of B7-H1 in human glioma cells in vitro and in vivo Although lacking B71/2 (CD80/86), all 12 glioma cell lines constitutively expressed B7-H1 mRNA and protein Exposure to IFN-γ strongly enhanced B7-H1 expression Immunohistochemical analysis of malignant glioma specimens revealed strong B7-H1 expression in all 10 samples examined, whereas no B7-H1 expression could be detected on normal brain tissues To elucidate the functional significance of glioma cell-related B7-H1 expression, we performed coculture experiments of glioma cells with alloreactive CD4+ and CD8+ T cells Glioma-related B7-H1 was identified as a strong inhibitor of CD4+ as well as CD8+ T-cell activation as assessed by increased cytokine production (IFN-γ, interleukin-2, and interleukin-10) and expression levels of the T-cell activation marker (CD69) in the presence of a neutralizing antibody against B7-H1 (mAb 5H1) B7-H1 expression may thus significantly influence the outcome of T-cell tumor cell interactions and represents a novel mechanism by which glioma cells evade immune recognition and destruction.

Original languageEnglish (US)
Pages (from-to)7462-7467
Number of pages6
JournalCancer Research
Volume63
Issue number21
StatePublished - Nov 1 2003
Externally publishedYes

Fingerprint

B7 Antigens
Glioma
Paralysis
T-Lymphocytes
Glioblastoma
Coculture Techniques
Neutralizing Antibodies
Cell Communication
Interleukin-10
Interleukin-2
Neoplasms
Cytokines
Cell Line
Messenger RNA
Brain

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Wintterle, S., Schreiner, B., Mitsdoerffer, M., Schneider, D., Chen, L., Meyermann, R., ... Wiendl, H. (2003). Expression of the B7-Related Molecule B7-H1 by Glioma Cells: A Potential Mechanism of Immune Paralysis. Cancer Research, 63(21), 7462-7467.

Expression of the B7-Related Molecule B7-H1 by Glioma Cells : A Potential Mechanism of Immune Paralysis. / Wintterle, Sabine; Schreiner, Bettina; Mitsdoerffer, Meike; Schneider, Dagmar; Chen, Lieping; Meyermann, Richard; Weller, Michael; Wiendl, Heinz.

In: Cancer Research, Vol. 63, No. 21, 01.11.2003, p. 7462-7467.

Research output: Contribution to journalArticle

Wintterle, S, Schreiner, B, Mitsdoerffer, M, Schneider, D, Chen, L, Meyermann, R, Weller, M & Wiendl, H 2003, 'Expression of the B7-Related Molecule B7-H1 by Glioma Cells: A Potential Mechanism of Immune Paralysis', Cancer Research, vol. 63, no. 21, pp. 7462-7467.
Wintterle S, Schreiner B, Mitsdoerffer M, Schneider D, Chen L, Meyermann R et al. Expression of the B7-Related Molecule B7-H1 by Glioma Cells: A Potential Mechanism of Immune Paralysis. Cancer Research. 2003 Nov 1;63(21):7462-7467.
Wintterle, Sabine ; Schreiner, Bettina ; Mitsdoerffer, Meike ; Schneider, Dagmar ; Chen, Lieping ; Meyermann, Richard ; Weller, Michael ; Wiendl, Heinz. / Expression of the B7-Related Molecule B7-H1 by Glioma Cells : A Potential Mechanism of Immune Paralysis. In: Cancer Research. 2003 ; Vol. 63, No. 21. pp. 7462-7467.
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