Disruption of membrane cholesterol stimulates MyD88-dependent NF-kappaB activation in immature B cells.
Cell Immunol
; 229(1): 68-77, 2004 May.
Article
em En
| MEDLINE
| ID: mdl-15331330
ABSTRACT
Agents that extract or sequester membrane cholesterol stimulate IkappaB degradation and lead to NF-kappaB activation in a subset of B cells. Although the extraction of cholesterol by methyl-beta-cyclodextrin is the most potent stimulus of NF-kappaB, other agents that sequester cholesterol have similar effects. B cells and B cell lines with an immature phenotype are significantly more sensitive to the effects of cholesterol perturbation than their mature B cell counterparts. NF-kappaB activation does not involve signaling from the B cell receptor complex. Instead, the disruption of membrane cholesterol activates NF-kappaB through a MyD88-dependent pathway involving the pattern recognition receptor, Toll-like receptor 4. We suggest that lipid raft microdomains may serve not only to orchestrate receptor signaling, but to sequester signaling components one from one another, which serves to prevent receptor-mediated signaling from occurring. A role for this process during B cell development is suggested.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Linfócitos B
/
Ativação Linfocitária
/
Receptores Imunológicos
/
Antígenos de Diferenciação
/
Colesterol
/
NF-kappa B
Limite:
Animals
Idioma:
En
Revista:
Cell Immunol
Ano de publicação:
2004
Tipo de documento:
Article
País de afiliação:
Estados Unidos