Fas ligand expression by astrocytoma in vivo: maintaining immune privilege in the brain?

P Saas; P R Walker; M Hahne; A L Quiquerez; V Schnuriger; G Perrin; L French; E G Van Meir; N de Tribolet; J Tschopp; P Y Dietrich

doi:10.1172/JCI119273

Division of Oncology, University Hospital, Geneva, Switzerland.

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Division of Oncology, University Hospital, Geneva, Switzerland.

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Division of Oncology, University Hospital, Geneva, Switzerland.

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Division of Oncology, University Hospital, Geneva, Switzerland.

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Division of Oncology, University Hospital, Geneva, Switzerland.

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Division of Oncology, University Hospital, Geneva, Switzerland.

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Division of Oncology, University Hospital, Geneva, Switzerland.

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Division of Oncology, University Hospital, Geneva, Switzerland.

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Division of Oncology, University Hospital, Geneva, Switzerland.

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Division of Oncology, University Hospital, Geneva, Switzerland.

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Division of Oncology, University Hospital, Geneva, Switzerland.

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Published in Volume 99, Issue 6 on March 15, 1997
J Clin Invest. 1997;99(6):1173–1178. https://doi.org/10.1172/JCI119273.
© 1997 The American Society for Clinical Investigation

Published March 15, 1997 - Version history

Astrocytomas are among the most common brain tumors that are usually fatal in their malignant form. They appear to progress without significant impedance from the immune system, despite the presence of intratumoral T cell infiltration. To date, this has been thought to be the result of T cell immunosuppression induced by astrocytoma-derived cytokines. Here, we propose that cell contact-mediated events also play a role, since we demonstrate the in vivo expression of Fas ligand (FasL/CD95L) by human astrocytoma and the efficient killing of Fas-bearing cells by astrocytoma lines in vitro and by tumor cells ex vivo. Functional FasL is expressed by human, mouse, and rat astrocytoma and hence may be a general feature of this nonlymphoid tumor. In the brain, astrocytoma cells can potentially deliver a death signal to Fas+ cells which include infiltrating leukocytes and, paradoxically, astrocytoma cells themselves. The expression of FasL by astrocytoma cells may extend the processes that are postulated to occur in normal brain to maintain immune privilege, since we also show FasL expression by neurons. Overall, our findings suggest that FasL-induced apoptosis by astrocytoma cells may play a significant role in both immunosuppression and the regulation of tumor growth within the central nervous system.

Version 1 (March 15, 1997): No description

Fas ligand expression by astrocytoma in vivo: maintaining immune privilege in the brain?

P Saas, P R Walker, M Hahne, A L Quiquerez, V Schnuriger, G Perrin, L French, E G Van Meir, N de Tribolet, J Tschopp, and P Y Dietrich

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Fas ligand expression by astrocytoma in vivo: maintaining immune privilege in the brain?

P Saas, P R Walker, M Hahne, A L Quiquerez, V Schnuriger, G Perrin, L French, E G Van Meir, N de Tribolet, J Tschopp, and P Y Dietrich

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