Dane Parker
Editor

2014

Type I interferon (IFN) signaling has long been recognized as a critical component of innate immune defense to viral pathogens. It is now established that bacteria too are able to activate this pathway. Typically bacteria activate type I IFN signaling through TLR-dependent mechanisms, through recognition of LPS in Gram negative organisms or via TLRs and cytosolic receptors that respond to nucleic acids and messaging molecules that are either endocytosed or secreted directly into the eukaryotic cells. The consequences of type I IFN signaling on host outcome can be either protective or damaging, depending on the organism.