Chlamydia pneumoniae impairs the innate immune response in infected epithelial cells by targeting TRAF3.

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-β production. Instead, infected cells are prevented from activati

SUBMITTER: Wolf K 

PROVIDER: S-EPMC3563728 | biostudies-literature | 2013 Feb

REPOSITORIES: biostudies-literature