Abstract
TWEAK is a member of the TNF family, constitutively expressed in the central nervous system (CNS), with pro-inflammatory, proliferative or apoptotic effects depending upon cell types. Its receptor, Fn14, is expressed in CNS by endothelial cells, reactive astrocytes and neurons. We showed that TWEAK and Fn14 mRNA expression increased in spinal cord during experimental autoimmune encephalomyelitis (EAE). We investigated the role of TWEAK during EAE using neutralizing anti-TWEAK antibody in myelin oligodendrocyte glycoprotein (MOG) induced EAE in C57BL/6 mice. We observed a reduction of disease severity and leukocyte infiltration when mice were treated after the priming phase.
MeSH terms
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Animals
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Antibodies, Monoclonal / therapeutic use*
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Apoptosis Regulatory Proteins
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Astrocytes / drug effects
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Brain / drug effects*
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Brain / immunology
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Brain / pathology
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Carrier Proteins / immunology*
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Carrier Proteins / metabolism
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Cell Movement / drug effects
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Cells, Cultured
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Cytokine TWEAK
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Encephalomyelitis, Autoimmune, Experimental / drug therapy*
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Encephalomyelitis, Autoimmune, Experimental / pathology
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Humans
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Mice
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Reverse Transcriptase Polymerase Chain Reaction
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Spinal Cord / drug effects*
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Spinal Cord / immunology
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Spinal Cord / pathology
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T-Lymphocytes / drug effects
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T-Lymphocytes / immunology
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Time Factors
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Tumor Necrosis Factors
Substances
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Antibodies, Monoclonal
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Apoptosis Regulatory Proteins
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Carrier Proteins
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Cytokine TWEAK
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Tnfsf12 protein, mouse
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Tumor Necrosis Factors