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

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 p75NTR in CNS endothelial cells during inflammation and involvement in preservation of blood-brain barrier integrity during a severe infiltrative attack.

Original languageEnglish
Pages (from-to)41-53
Number of pages13
JournalJournal of Neuroimmunology
Volume148
Issue number1-2
DOIs
Publication statusPublished - Mar 2004

Cite this

Copray, Sjef ; Küst, Britta ; Emmer, Bart ; Lin, May Young ; Liem, Robert ; Amor, Sandra ; de Vries, Helga ; Floris, Sarah ; Boddeke, Erik. / Deficient p75 low-affinity neurotrophin receptor expression exacerbates experimental allergic encephalomyelitis in C57/BL6 mice. In: Journal of Neuroimmunology. 2004 ; Vol. 148, No. 1-2. pp. 41-53.
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title = "Deficient p75 low-affinity neurotrophin receptor expression exacerbates experimental allergic encephalomyelitis in C57/BL6 mice",
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 p75NTR in CNS endothelial cells during inflammation and involvement in preservation of blood-brain barrier integrity during a severe infiltrative attack.",
keywords = "Animals, Blood Vessels, CD11 Antigens, CD3 Complex, Central Nervous System, Disease Models, Animal, Encephalomyelitis, Autoimmune, Experimental, Endothelial Cells, Gene Expression, Glycoproteins, Immunization, Immunohistochemistry, Mice, Mice, Inbred C57BL, Mice, Knockout, Microscopy, Electron, Multiple Sclerosis, Myelin-Oligodendrocyte Glycoprotein, Peptide Fragments, Probability, Receptor, Nerve Growth Factor, Receptors, Nerve Growth Factor, Time Factors, Comparative Study, Journal Article, Research Support, Non-U.S. Gov't",
author = "Sjef Copray and Britta K{\"u}st and Bart Emmer and Lin, {May Young} and Robert Liem and Sandra Amor and {de Vries}, Helga and Sarah Floris and Erik Boddeke",
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Deficient p75 low-affinity neurotrophin receptor expression exacerbates experimental allergic encephalomyelitis in C57/BL6 mice. / Copray, Sjef; Küst, Britta; Emmer, Bart; Lin, May Young; Liem, Robert; Amor, Sandra; de Vries, Helga; Floris, Sarah; Boddeke, Erik.

In: Journal of Neuroimmunology, Vol. 148, No. 1-2, 03.2004, p. 41-53.

Research output: Contribution to journalArticleAcademicpeer-review

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AU - Copray, Sjef

AU - Küst, Britta

AU - Emmer, Bart

AU - Lin, May Young

AU - Liem, Robert

AU - Amor, Sandra

AU - de Vries, Helga

AU - Floris, Sarah

AU - Boddeke, Erik

PY - 2004/3

Y1 - 2004/3

N2 - 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 p75NTR in CNS endothelial cells during inflammation and involvement in preservation of blood-brain barrier integrity during a severe infiltrative attack.

AB - 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 p75NTR in CNS endothelial cells during inflammation and involvement in preservation of blood-brain barrier integrity during a severe infiltrative attack.

KW - Animals

KW - Blood Vessels

KW - CD11 Antigens

KW - CD3 Complex

KW - Central Nervous System

KW - Disease Models, Animal

KW - Encephalomyelitis, Autoimmune, Experimental

KW - Endothelial Cells

KW - Gene Expression

KW - Glycoproteins

KW - Immunization

KW - Immunohistochemistry

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Microscopy, Electron

KW - Multiple Sclerosis

KW - Myelin-Oligodendrocyte Glycoprotein

KW - Peptide Fragments

KW - Probability

KW - Receptor, Nerve Growth Factor

KW - Receptors, Nerve Growth Factor

KW - Time Factors

KW - Comparative Study

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

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SP - 41

EP - 53

JO - Journal of Neuroimmunology

JF - Journal of Neuroimmunology

SN - 0165-5728

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