Deficient p75 low-affinity neurotrophin receptor expression exacerbates experimental allergic encephalomyelitis in C57/BL6 mice

Sjef Copray, Britta Küst, Bart Emmer, May Young Lin, Robert Liem, Sandra Amor, Helga de Vries, Sarah Floris, Erik Boddeke

Research output: Contribution to journalArticleAcademicpeer-review

40 Citations (Scopus)

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 languageEnglish
Pages (from-to)41-53
Number of pages13
JournalJournal of Neuroimmunology
Volume148
Issue number1-2
DOIs
Publication statusPublished - 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

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