Abstract
The TNF-related apoptosis-inducing ligand (TRAIL) has well-described anti-inflammatory effects in models of autoimmune disease, including experimental autoimmune encephalomyelitis (EAE). In this issue of Neuron, Aktas, Smorodchenko, and colleagues present evidence that TRAIL exerts anti-inflammatory effects, but also induces neuronal apoptosis, in EAE. This report poses the therapeutic challenge of facilitating TRAIL expression in the periphery while inhibiting TRAIL in the CNS.
MeSH terms
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Animals
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Apoptosis Regulatory Proteins
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Encephalomyelitis, Autoimmune, Experimental / immunology
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Encephalomyelitis, Autoimmune, Experimental / metabolism*
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Humans
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Membrane Glycoproteins / immunology
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Membrane Glycoproteins / metabolism*
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Neurons / metabolism
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Neurons / pathology
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TNF-Related Apoptosis-Inducing Ligand
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Tumor Necrosis Factor-alpha / immunology
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Tumor Necrosis Factor-alpha / metabolism*
Substances
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Apoptosis Regulatory Proteins
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Membrane Glycoproteins
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TNF-Related Apoptosis-Inducing Ligand
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TNFSF10 protein, human
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Tumor Necrosis Factor-alpha