Continuous cuprizone intoxication allows active experimental autoimmune encephalomyelitis induction in C57BL/6 mice.
Multiple sclerosis
Neuroinflammation
Oligodendrocyte injury
Peripheral immune-cell recruitment
Journal
Histochemistry and cell biology
ISSN: 1432-119X
Titre abrégé: Histochem Cell Biol
Pays: Germany
ID NLM: 9506663
Informations de publication
Date de publication:
Aug 2019
Aug 2019
Historique:
accepted:
14
04
2019
pubmed:
25
4
2019
medline:
7
9
2019
entrez:
25
4
2019
Statut:
ppublish
Résumé
Oligodendrocyte degeneration is a hallmark of multiple sclerosis pathology, and protecting oligodendrocytes and myelin is likely to be of clinical relevance. Traditionally, oligodendrocyte and myelin degeneration are viewed as a direct consequence of an inflammatory attack, but metabolic defects might be equally important. Appropriate animal models to study the interplay of inflammation and metabolic injury are, therefore, needed. Here, we describe that in spite of its immunosuppressive effects, a continuous intoxication with cuprizone allows the induction of active experimental autoimmune encephalomyelitis (EAE) by myelin oligodendrocyte glycoprotein (MOG
Identifiants
pubmed: 31016368
doi: 10.1007/s00418-019-01786-4
pii: 10.1007/s00418-019-01786-4
doi:
Substances chimiques
Myelin-Oligodendrocyte Glycoprotein
0
Peptide Fragments
0
myelin oligodendrocyte glycoprotein (35-55)
0
Cuprizone
5N16U7E0AO
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
119-131Références
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