Abstract
Rheumatoid arthritis (RA) is one of the most prevalent autoimmune diseases. It is characterized by chronic inflammation of the joint leading to its destruction. Although the initiating cause remains elusive, environmental factors and genetic background are known to contribute to the etiology of RA. The role of Toll-like receptors (TLRs) in innate immunity and their ability to recognize microbial products has been well characterized. TLRs are able to recognize endogenous molecules released upon cell damage and necrosis, and are present in RA synovial fluid. Although it appears unlikely that a pathogen underlies the pathogenesis or progression of RA, the release of endogenous TLR ligands during inflammation may activate TLRs and perpetuate the disease. An increasing body of circumstantial evidence implicates TLR signaling in RA, although, at present, their involvement is not defined comprehensively. Targeting individual TLRs or their signaling transducers may provide a more specific therapy without global suppression of the immune system.
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