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A₁ Adenosine Receptors in Microglia Control Glioblastoma-Host Interaction

¹ Cellular Neuroscience Group, Max Delbrück Center for Molecular Medicine; ² Department of Neurosurgery, Helios Hospital Berlin; ³ Department of Psychiatry, Free University, Berlin, Germany; ⁴ National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland; and ⁵ Department of Molecular Cell Biology, Faculty of Medicine, Amsterdam, the Netherlands

Requests for reprints: Helmut Kettenmann, Max Delbrück Center for Molecular Medicine Berlin-Buch (MDC) Robert Rössle Strasse 10, 13092 Berlin, Germany. Phone: 49-30-9406-3325; Fax: 49-30-9406-3819; E-mail: kettenmann{at}mdc-berlin.de.

We report that experimental glioblastoma grow more vigorously in A₁ adenosine receptor (A₁AR)–deficient mice associated with a strong accumulation of microglial cells at and around the tumors. A₁ARs were prominently expressed in microglia associated with tumor cells as revealed with immunocytochemistry but low in microglia in the unaffected brain tissue. The A₁AR could also be detected on microglia from human glioblastoma resections. To study functional interactions between tumor and host cells, we studied glioblastoma growth in organotypical brain slice cultures. A₁AR agonists suppressed tumor growth. When, however, microglial cells were depleted from the slices, the agonists even stimulated tumor growth. Thus, adenosine attenuates glioblastoma growth acting via A₁AR in microglia. (Cancer Res 2006; 66(17): 8550-7)

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