Format

Send to

Choose Destination
See comment in PubMed Commons below
J Immunol. 2013 Feb 15;190(4):1695-701. doi: 10.4049/jimmunol.1202443. Epub 2013 Jan 9.

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

Author information

1
Department of Microbiology and Immunology, Miller School of Medicine, University of Miami, Miami, FL 33136, USA. kwolf@med.miami.edu

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 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.

PMID:
23303668
PMCID:
PMC3563728
DOI:
10.4049/jimmunol.1202443
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments

    Supplemental Content

    Full text links

    Icon for HighWire Icon for PubMed Central
    Loading ...
    Support Center