The role of toll-like receptors in chronic inflammation.
The role of Toll-like receptors (TLRs) in innate immunity and their ability to recognise microbial products has been well characterised. TLRs are also able to recognise endogenous molecules which are released upon cell damage and necrosis and have been shown to be present in numerous autoimmune diseases. Therefore, the release of endogenous TLR ligands during inflammation and consequently the activation of TLR signalling pathways may be one mechanism initiating and driving autoimmune diseases. An increasing body of circumstantial evidence implicates a role of TLR signalling in systemic lupus erythematosus (SLE), atherosclerosis, asthma, type 1 diabetes, multiple sclerosis, bowl inflammation and rheumatoid arthritis (RA). Although at present their involvement is not comprehensively defined. However, future therapies targeting individual TLRs or their signalling transducers may provide a more specific way of treating inflammatory diseases without global suppression of the immune system.
Drexler
Stefan K
SK
Kennedy Institute of Rheumatology Division, Faculty of Medicine, Imperial College of Science, Technology and Medicine, 1 Aspenlea Road, Hammersmith, London W6 8LH, UK. Stefan.Drexler@unil.ch <Stefan.Drexler@unil.ch>
Foxwell
Brian M
BM
D000276:Adjuvants, Immunologic; D000818:Animals; D001327:Autoimmune Diseases / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D002908:Chronic Disease; D020022:Genetic Predisposition to Disease; D006801:Humans; D007108:Immune Tolerance; D007249:Inflammation; D035683:MicroRNAs / Q000276:immunology; D009369:Neoplasms / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D011110:Polymorphism, Genetic; D015398:Signal Transduction / Q000276:immunology; D051193:Toll-Like Receptors / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D019139:Tumor Escape
D000276:Adjuvants, Immunologic; D035683:MicroRNAs; D051193:Toll-Like Receptors