Abstract
We have investigated the role of p75NTR in inflammation in experimental allergic encephalomyelitis (EAE), a model for the human disease multiple sclerosis (MS). Induction of EAE in C57/BL6 wild-type mice resulted in expression of p75NTR in endothelial cells in the CNS. In contrast to the clinical manifestation of EAE observed in wild-type C57/BL6 mice, mice deficient for p75NTR (p75NTR knockout mice) developed severe or lethal disease and concomitant increased levels of inflammation in the CNS. Our findings suggest a physiological significant role for p75 NTR in CNS endothelial cells during inflammation and involvement in preservation of blood-brain barrier integrity during a severe infiltrative attack. © 2003 Elsevier B.V. All rights reserved.
Original language | English |
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Pages (from-to) | 41-53 |
Number of pages | 13 |
Journal | Journal of Neuroimmunology |
Volume | 148 |
Issue number | 1-2 |
DOIs | |
Publication status | Published - Mar 2004 |
Keywords
- Animals
- Blood Vessels
- CD11 Antigens
- CD3 Complex
- Central Nervous System
- Comparative Study
- Disease Models, Animal
- Encephalomyelitis, Autoimmune, Experimental
- Endothelial Cells
- Gene Expression
- Glycoproteins
- Immunization
- Immunohistochemistry
- Journal Article
- Mice
- Mice, Inbred C57BL
- Mice, Knockout
- Microscopy, Electron
- Multiple Sclerosis
- Myelin-Oligodendrocyte Glycoprotein
- Peptide Fragments
- Probability
- Receptor, Nerve Growth Factor
- Receptors, Nerve Growth Factor
- Research Support, Non-U.S. Gov't
- Time Factors