ABSTRACT
Innate immune activation triggered by viral single-stranded RNA is mediated by Toll-like receptors 7 and 8, and leads to the induction of type I interferons and other pro-inflammatory cytokines. Interferon production in response to single-stranded RNA ligands is restricted to plasmacytoid dendritic cells and is largely mediated by Toll-like receptor 7, while pro-inflammatory cytokines such as interleukins 6 and 12 are produced by myeloid dendritic cells that express mainly Toll-like receptor 8. In both cases, ligand recognition takes place in a specialized endosomal compartment and is therefore similar to the recognition of bacterial and viral DNA by Toll-like receptor 9. Recognition of single-stranded RNA appears largely sequenceindependent and consequently, self RNA can act as an agonist. Recognition of self RNA and DNA plays a role in the progression of autoimmune diseases such as systemic lupus erythematosus. The conditions that allow self RNA to gain access to the endosomal compartments mediating single-stranded RNA recognition, and the extent to which such interactions are involved in initiating autoimmune responses, are currently unclear.
