Toll-like receptors and NOD-like receptors in rheumatic diseases 英文参考文献.docVIP

Available online /content/11/5/243 Review Toll-like receptors and NOD-like receptors in rheumatic diseases William J McCormack1, Andrew E Parker1 and Luke A O’Neill2 1OPSONA Therapeutics Ltd, Institute of Molecular Medicine, Trinity Centre for Health Sciences, St James’ Hospital, Dublin 8, Ireland 2School of Biochemistry Immunology, Trinity College Dublin, College Green, Dublin 2, Ireland Corresponding author: Luke A O’Neill, laoneill@tcd.ie Published: 14 October 2009 Arthritis Research Therapy 2009, 11:243 (doi:10.1186/ar2729) This article is online at /content/11/5/243 ? 2009 BioMed Central Ltd Abstract In the present review we will summarise the current state of knowledge in TLRs and NLRs, and also speculate on their roles in the pathogenesis of autoinflammatory joint diseases. The past 10 years have seen the description of families of receptors that drive proinflammatory cytokine production in infection and tissue injury. Two major classes have been examined in the context of inflammatory joint disease – the Toll-like receptors (TLRs) and NOD-like receptors (NLRs). TLRs such as TLR2 and TLR4 are being implicated in the pathology of rheumatoid arthritis, ankylosing spondylitis, lyme arthritis and osteoarthritis. Nalp3 has been identified as a key NLR for IL-1β production and has been shown to have a particular role in gout. These findings present new therapeutic opportunities, possibly allowing for the replacement of biologics with small molecule inhibitors. Toll-like receptors The past 10 years have seen over 11,000 papers published on TLRs, which is a testament to the importance placed upon them by inflammation biologists and immunologists. Ten TLRs occur in humans, and the roles of nine of them (TLR1 to TLR9) have been determined [1]. TLR2 senses lipopeptides from bacteria, with TLR1/2 dimers sensing triacylated lipopeptides and TLR2/6 dimers sensing diacylated lipopept