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The interferon response to bacterial and viral infections

Department of Microbiology, Immunology and Molecular Genetics, University of California Los Angeles, Los Angeles, California, USA

Supriya K. Saha

Department of Microbiology, Immunology and Molecular Genetics, University of California Los Angeles, Los Angeles, California, USA, Medical Scientist Training Program, University of California Los Angeles, Los Angeles, California, USA

Genhong Cheng

Department of Microbiology, Immunology and Molecular Genetics, University of California Los Angeles, Los Angeles, California, USA, genhongc{at}microbio.ucla.edu, Molecular Biology Institute, University of California Los Angeles, Los Angeles, California, USA, Jonsson Comprehensive Cancer Center, University of California Los Angeles, Los Angeles, California, USA

Type I interferons (IFNs) were first described several decades ago as soluble factors that were capable of `interfering' with viral replication when added to infected cells. Type I IFNs have been shown to be induced by recognition of viral DNA and RNA via three distinct pathways: (i) a TRIFdependent pathway in macrophages via TLRs 3 and 4; (ii) a MyD88-dependent pathway in plasmacytoid dendritic cells (pDCs) via TLRs 7/8 and 9; and (iii) an intracellular recognition pathway utilizing the cytoplasmic receptors RIG-I/MDA5. Interestingly, these viral recognition pathways converge on TRAF3, which induces interferon through the activation of IRF3 or IRF7 by the TBK-1 and IKKi complexes. While type I IFN has been traditionally associated with antiviral responses, recent studies have demonstrated that many bacteria also induce type I interferon responses. The mechanisms of type I IFN induction and its role in host defense, however, are largely unclear. Studies with the Gram-positive intracellular bacterium Listeria monocytogenes indicated that it may trigger type I IFN induction through novel TLR-independent intracellular receptors and type I IFN may play a detrimental role to host response against listerial infection. In this article, we summarize some of these findings and discuss the functional differences of type I IFNs in bacterial and viral infections.

Key Words: Bacteria • interferon • TLR • TRAF3 • virus

Journal of Endotoxin Research, Vol. 12, No. 4, 246-250 (2006)
DOI: 10.1177/09680519060120040601


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