title: [Innate immunity, autoimmunity and autoinflammation].
abstract: T and B lymphocytes of the acquired immune system are functionally superimposed on the evolutionary old innate immune system. The latter recognizes conserved microbial structures through pattern recognition receptors (PRR) which are coactivated by "danger" signals through cytoplasmic PRR termed NOD-like receptors (NLR). These signals include nuclear fragments released by stressed or dying cells. NLR-signalling activates the enzyme caspase-1, which is required for release of pro-inflammatory cytokines such as interleukin (IL)-1ß, IL-18 and IL-33. Dysfunction of innate immunity is central to autoinflammation and may contribute to autoimmunity.
authors.affiliation: Institut for Inflammationsforskning, Finsencentret, Rigshospitalet, Blegdamsvej 9, 2100 København Ø, Denmark. klausben@me.com
authors.forename: Klaus
authors.initials: K
authors.lastname: Bendtzen
mesh_terms: D001327:Autoimmune Diseases / Q000276:immunology*; D015551:Autoimmunity / Q000502:physiology; D001402:B-Lymphocytes / Q000276:immunology; D056660:Hereditary Autoinflammatory Diseases / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate / Q000502:physiology; D007249:Inflammation / Q000276:immunology*; D051192:Receptors, Pattern Recognition / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D051192:Receptors, Pattern Recognition