Powered by OpenAIRE graph
image/svg+xml Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Closed Access logo, derived from PLoS Open Access logo. This version with transparent background. http://commons.wikimedia.org/wiki/File:Closed_Access_logo_transparent.svg Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Amsterdam UMC (VU Am...arrow_drop_down
image/svg+xml Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Closed Access logo, derived from PLoS Open Access logo. This version with transparent background. http://commons.wikimedia.org/wiki/File:Closed_Access_logo_transparent.svg Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao
image/svg+xml Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Closed Access logo, derived from PLoS Open Access logo. This version with transparent background. http://commons.wikimedia.org/wiki/File:Closed_Access_logo_transparent.svg Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao
Journal of Neuroimmunology
Article . 2004 . Peer-reviewed
License: Elsevier TDM
Data sources: Crossref
versions View all 4 versions

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

Authors: Copray, Sjef; Küst, Britta; Emmer, Bart; Lin, May Young; Liem, Robert; Amor, Sandra; de Vries, Helga; +2 Authors

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

Central Nervous System, Encephalomyelitis, Autoimmune, Experimental, Multiple Sclerosis, CD3 Complex, Gene Expression, myelin oligodendrocyte glycoprotein, multiple sclerosis, Mice, MYELIN OLIGODENDROCYTE GLYCOPROTEIN, Animals, Glycoproteins, Probability, Mice, Knockout, CD11 Antigens, experimental allergic encephalomyelitis, NERVE GROWTH-FACTOR, DEATH, Endothelial Cells, BASIC-PROTEIN, Immunohistochemistry, Peptide Fragments, P75(NTR), Mice, Inbred C57BL, Disease Models, Animal, Microscopy, Electron, inflammation, EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS, CELLS, endothelial cell, Blood Vessels, Immunization, Myelin-Oligodendrocyte Glycoprotein, SPINAL-CORD, MESSENGER-RNA, SYSTEM

  • BIP!
    Impact byBIP!
    citations
    This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    44
    popularity
    This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
    Top 10%
    influence
    This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    Top 10%
    impulse
    This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
    Top 10%
Powered by OpenAIRE graph
citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
44
Top 10%
Top 10%
Top 10%