title: The interferon in TLR signaling: more than just antiviral.
abstract: The Toll-like receptor (TLR) system is responsible for the recognition of infectious agents leading to initiation of the primary innate, and later adaptive, immune response. Genetic technologies have enabled the discovery of new factors involved in these systems, their genetic manipulation and the global analyses of their effects on gene expression. Furthermore, this increased understanding has resulted in the need to reassess our preconceptions about the functions of well-known molecules. For example, type I interferons (IFNs), which were discovered as antiviral proteins, are now known to be produced in response to TLR activation by many pathogens, including bacteria. Should we be surprised? Has the inflammatory response unexpectedly highjacked the body's antiviral system? Or are we too easily blinkered by preconceptions from how a compound was discovered?
authors.affiliation: Centre for Functional Genomics and Human Disease, Monash Institute of Reproduction and Development, Monash University, Clayton, Victoria 3168, Australia. paul.hertzog@med.monash.edu.au
authors.forename: Paul J
authors.initials: PJ
authors.lastname: Hertzog
authors.forename: Luke A
authors.initials: LA
authors.lastname: O'Neill
authors.forename: John A
authors.initials: JA
authors.lastname: Hamilton
mesh_terms: D000818:Animals; D001419:Bacteria / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate; D007370:Interferon Type I / Q000502:physiology*; D008562:Membrane Glycoproteins / Q000502:physiology*; D011956:Receptors, Cell Surface / Q000502:physiology*; D015398:Signal Transduction / Q000276:immunology*; D051193:Toll-Like Receptors; D014780:Viruses / Q000276:immunology
chemical_list: D007370:Interferon Type I; D008562:Membrane Glycoproteins; D011956:Receptors, Cell Surface; D051193:Toll-Like Receptors