title: Nucleic acid-sensing TLRs as modifiers of autoimmunity.
abstract: The immune system requires precise regulation of activating and inhibitory signals so that it can mount effective responses against pathogens while ensuring tolerance to self-components. Some of the most potent activation signals are triggered by innate immune molecules, particularly those in the TLR family. Recent studies have shown that engagement of TLRs plays a significant role in both innate and adaptive immunity. This review focuses on the ways that TLR function might contribute to the etiology of lupus-like syndromes in the context of an autoimmune-prone environment. By considering the sources, localization, and expression of both nucleic acids and the molecules that bind them, we discuss several ways that innate immunity can play a role in the development of systemic autoimmunity.
authors.affiliation: Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA.
authors.forename: Jonathan A
authors.initials: JA
authors.lastname: Deane
authors.forename: Silvia
authors.initials: S
authors.lastname: Bolland
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases / Q000235:genetics* / Q000276:immunology* / Q000378:metabolism; D004247:DNA / Q000276:immunology* / Q000378:metabolism; D006801:Humans; D007113:Immunity, Innate / Q000235:genetics; D012313:RNA / Q000276:immunology* / Q000378:metabolism; D051193:Toll-Like Receptors / Q000235:genetics / Q000378:metabolism / Q000502:physiology*
chemical_list: D051193:Toll-Like Receptors; D012313:RNA; D004247:DNA