Signaling pathways activated by microorganisms.
Invasion of viruses and bacteria is initially sensed by the host innate immune system, and evokes a rapid inflammatory response. Nucleotides from RNA viruses are recognized by retinoic-acid-inducible gene I-like helicases and Toll-like receptors, and this recognition triggers signaling cascades that induce antiviral mediators such as type I interferons. By contrast, Toll-like receptors recognizing bacterial components induce the expression of proinflammatory cytokines. Furthermore, recent studies suggest that viral and bacterial DNA also induce interferons in a Toll-independent mechanism, possibly through unidentified cytoplasmic receptor(s).
Takeuchi
Osamu
O
Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, ERATO, Japan Science and Technology Agency, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan.
Akira
Shizuo
S
D000818:Animals; D018407:Bacterial Physiological Phenomena; D053487:DEAD-box RNA Helicases / Q000378:metabolism; D004269:DNA, Bacterial / Q000378:metabolism; D004279:DNA, Viral / Q000378:metabolism; D006801:Humans; D007113:Immunity, Innate; D007370:Interferon Type I / Q000378:metabolism; D008954:Models, Biological; D012328:RNA Viruses / Q000378:metabolism / Q000502:physiology*; D011956:Receptors, Cell Surface / Q000378:metabolism; D015398:Signal Transduction; D051193:Toll-Like Receptors / Q000378:metabolism
D004269:DNA, Bacterial; D004279:DNA, Viral; D007370:Interferon Type I; D011956:Receptors, Cell Surface; D051193:Toll-Like Receptors; D053487:DEAD-box RNA Helicases