Caspase-11 mediates oligodendrocyte cell death and pathogenesis of autoimmune-mediated demyelination.
J Exp Med
; 193(1): 111-22, 2001 Jan 01.
Article
em En
| MEDLINE
| ID: mdl-11136825
ABSTRACT
Multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), are inflammatory diseases of the central nervous system (CNS) characterized by localized areas of demyelination. The mechanisms underlying oligodendrocyte (OLG) injury in MS and EAE remain unknown. Here we show that caspase-11 plays crucial roles in OLG death and pathogenesis in EAE. Caspase-11 and activated caspase-3 were both expressed in OLGs in spinal cord EAE lesions. OLGs from caspase-11-deficient mice were highly resistant to the cell death induced by cytotoxic cytokines. EAE susceptibility and cytokine concentrations in the CNS were significantly reduced in caspase-11-deficient mice. Our findings suggest that OLG death is mediated by a pathway that involves caspases-11 and -3 and leads to the demyelination observed in EAE.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Oligodendroglia
/
Caspases
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Encefalomielite Autoimune Experimental
Tipo de estudo:
Etiology_studies
/
Prognostic_studies
Limite:
Animals
/
Female
/
Humans
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Male
/
Pregnancy
Idioma:
En
Revista:
J Exp Med
Ano de publicação:
2001
Tipo de documento:
Article
País de afiliação:
Japão