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).
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