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. 2005 May 5;46(3):421-32.
doi: 10.1016/j.neuron.2005.03.018.

Neuronal damage in autoimmune neuroinflammation mediated by the death ligand TRAIL

Orhan Aktas  1 , Alina Smorodchenko, Stefan Brocke, Carmen Infante-Duarte, Ulf Schulze Topphoff, Johannes Vogt, Timour Prozorovski, Susanne Meier, Venera Osmanova, Elena Pohl, Ingo Bechmann, Robert Nitsch, Frauke Zipp
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Free article

Neuronal damage in autoimmune neuroinflammation mediated by the death ligand TRAIL

Orhan Aktas et al. Neuron. .
Free article

Abstract

Here, we provide evidence for a detrimental role of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in neural death in T cell-induced experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). Clinical severity and neuronal apoptosis in brainstem motor areas were substantially reduced upon brain-specific blockade of TRAIL after induction of EAE through adoptive transfer of encephalitogenic T cells. Furthermore, TRAIL-deficient myelin-specific lymphocytes showed reduced encephalitogenicity when transferred to wild-type mice. Conversely, intracerebral delivery of TRAIL to animals with EAE increased clinical deficits, while naive mice were not susceptible to TRAIL. Using organotypic slice cultures as a model for living brain tissue, we found that neurons were susceptible to TRAIL-mediated injury induced by encephalitogenic T cells. Thus, in addition to its known immunoregulatory effects, the death ligand TRAIL contributes to neural damage in the inflamed brain.

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  • Taking two TRAILS.
    Ransohoff RM, Trapp BD. Ransohoff RM, et al. Neuron. 2005 May 5;46(3):355-6. doi: 10.1016/j.neuron.2005.04.028. Neuron. 2005. PMID: 15882629 Review.

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