title: Controlling systems of nucleic acid sensing-TLRs restrict homeostatic inflammation.
abstract: Nucleic acid sensing-TLRs recognize pathogen-derived nucleic acids (NAs) and induce anti-microbial immune responses. NA-sensing TLRs are reported to have a risk of mistakenly responding to self-derived NAs and causing a variety of autoimmune diseases. To warrant innate immune responses without detrimental inflammation, NA-sensing TLRs need to be tightly controlled in multiple aspects including expression and downstream signaling pathways. Along this line, TLR7 vs 9 balance has emerged as a new mechanism that controls activation of RNA-sensor TLR7. In this review, we discuss mechanisms controlling NA-sensing TLRs and autoimmune diseases as consequences of the dysregulated control mechanisms.
authors.affiliation: Division of Infectious Genetics, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
authors.forename: Ryutaro
authors.initials: R
authors.lastname: Fukui
authors.forename: Kensuke
authors.initials: K
authors.lastname: Miyake
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology; D006706:Homeostasis; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation / Q000276:immunology*; D051379:Mice; D018448:Models, Immunological; D009696:Nucleic Acids / Q000276:immunology*; D015398:Signal Transduction; D051199:Toll-Like Receptor 7 / Q000276:immunology / Q000378:metabolism; D051217:Toll-Like Receptor 9 / Q000276:immunology / Q000378:metabolism; D051193:Toll-Like Receptors / Q000276:immunology* / Q000378:metabolism
chemical_list: D009696:Nucleic Acids; D051199:Toll-Like Receptor 7; D051217:Toll-Like Receptor 9; D051193:Toll-Like Receptors