Chlamydia pneumoniae impairs the innate immune response in infected epithelial cells by targeting TRAF3.
J Immunol
; 190(4): 1695-701, 2013 Feb 15.
Article
em En
| MEDLINE
| ID: mdl-23303668
ABSTRACT
Type I IFNs are induced during microbial infections and have well-characterized antiviral activities. TRAF3 is a signaling molecule crucial for type I IFN production and, therefore, represents a potential target for disarming immune responses. Chlamydia pneumoniae is a human pathogen that primarily infects respiratory epithelial cells; the onset of symptoms takes several weeks, and the course of infection is protracted. C. pneumoniae has also been associated with a variety of chronic inflammatory conditions. Thus, typical C. pneumoniae infections of humans are consistent with an impairment in inflammatory responses to the microorganism. We demonstrate that infection of epithelial cells with C. pneumoniae does not lead to IFN-ß production. Instead, infected cells are prevented from activating IFN regulatory factor 3. This effect is mediated by C. pneumoniae-dependent degradation of TRAF3, which is independent of a functional proteasome. Hence, it is likely that C. pneumoniae expresses a unique protease targeting TRAF3-dependent immune effector mechanisms.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Regulação para Baixo
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Chlamydophila pneumoniae
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Mucosa Respiratória
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Fator 3 Associado a Receptor de TNF
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Imunidade Inata
Limite:
Humans
Idioma:
En
Revista:
J Immunol
Ano de publicação:
2013
Tipo de documento:
Article
País de afiliação:
Estados Unidos