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Brain, Vol. 125, No. 11, 2469-2480, November 2002
© 2002 Oxford University Press

TRAIL induces death of human oligodendrocytes isolated from adult brain

Mariola Matysiak1, Anna Jurewicz1, Dariusz Jaskolski2 and Krzysztof Selmaj1

1 Departments of Neurology and 2 Neurosurgery, Medical University of Lodz, Poland

Correspondence to: Krzysztof Selmaj, MD, PhD, Department of Neurology, Medical University of Lodz, 22 Kopcinskiego Street, 90-153 Lodz, Poland E-mail: kselmaj{at}afazja.am.lodz.pl

Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) has been reported to induce apoptosis in various tumour cell lines and, recently, also in normal cells. TRAIL interacts with four receptors: two signalling receptors (TRAIL-R1 and TRAIL-R2) and two decoy receptors (TRAIL-R3 and TRAIL-R4). We have shown that both signalling receptors are present on the surface of oligodendrocytes isolated from adult human brain (ahOL), whereas the decoy receptors are expressed at a low level on ahOL. TRAIL induces ahOL apoptosis—as characterized by Annexin V staining prior to propidium iodide cell uptake—under conditions of protein synthesis inhibition. However, pre-treatment of ahOL with interferon {gamma} (IFN{gamma}) evoked susceptibility to TRAIL-induced death, which did not require inhibition of protein synthesis. A blocking experiment with monoclonal antibodies directed against TRAIL-R1 and TRAIL-R2 revealed that TRAIL-R1 is mainly involved in TRAIL-induced apoptosis of ahOL. In contrast to ahOL, microglial cells were completely resistant to cell death induced by TRAIL. Microglial cells had high surface expression of the decoy receptor TRAIL-R3, suggesting that resistance of these glial cells to TRAIL-induced death depends on the presence of the protective effect of TRAIL-R3. Stimulation of microglia with TRAIL increased further expression of TRAIL-R3, but it had no effect on the expression of TRAIL receptors by ahOL. This result may implicate TRAIL as an effector-immune molecule in selective ahOL demise in inflammatory/demyelinating conditions.


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