Cathepsin C modulates myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis.
cathepsin C
cystatin F
demyelination
experimental autoimmune encephalomyelitis (EAE)
multiple sclerosis
Journal
Journal of neurochemistry
ISSN: 1471-4159
Titre abrégé: J Neurochem
Pays: England
ID NLM: 2985190R
Informations de publication
Date de publication:
02 2019
02 2019
Historique:
received:
15
01
2018
revised:
15
08
2018
accepted:
16
08
2018
pubmed:
29
8
2018
medline:
28
10
2019
entrez:
29
8
2018
Statut:
ppublish
Résumé
Multiple sclerosis (MS) is an autoimmune disease characterized by immune-mediated inflammation, which attacks the myelin sheath. MS pursues a relapsing and remitting course with varying intervals between symptoms. The main clinical pathological features include inflammation, myelin sheath destruction and plaque formation in the central nervous system (CNS). We previously reported that cystatin F (CysF) expression is induced in demyelinating lesions that are accompanied by active remyelination (referred to as shadow plaques) but is down-regulated in chronic demyelinated lesions (plaques) in the spinal cord of MS patients and in several murine models of demyelinating disease. CysF is a cathepsin protease inhibitor whose major target is cathepsin C (CatC), which is co-expressed in demyelinating regions in Plp
Substances chimiques
Cystatins
0
Myelin-Oligodendrocyte Glycoprotein
0
cystatin F, mouse
0
Cathepsin C
EC 3.4.14.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
413-425Informations de copyright
© 2018 International Society for Neurochemistry.