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This article is part of a series on The Scientific Basis of Rheumatology: A Decade of Progress, edited by Peter Lipsky and Ravinder Maini.

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Toll-like receptors and NOD-like receptors in rheumatic diseases

William J McCormack1 email, Andrew E Parker1 email and Luke A O'Neill2 email

OPSONA Therapeutics Ltd, Institute of Molecular Medicine, Trinity Centre for Health Sciences, St James' Hospital, Dublin 8, Ireland

School of Biochemistry & Immunology, Trinity College Dublin, College Green, Dublin 2, Ireland

author email corresponding author email

Arthritis Research & Therapy 2009, 11:243doi:10.1186/ar2729

Published: 14 October 2009

Abstract

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.


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