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Toll-like Receptor -A Potent Driving Force behind Rheumatoid Arthritis-

Journal

Publisher

JAPANESE SOC LYMPHORETICULAR TISSUE RESEARCH
DOI: 10.3960/jslrt.51.77

Keywords

Toll-like receptor; rheumatoid arthritis; pathogen-associated molecular pattern; damage-associated molecular pattern; innate immunity

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Funding

  1. Ministry of Science and Culture [C 2-17591546, C-21591929]
  2. Yamagata Health Support Society for the Promotion of Science, Japan

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Toll like receptor (TLR), one of the key functions of innate immune system, can recognize not only exogenous pathogen-associated molecular patterns, namely PAMPs, but also endogenous molecules created upon tissue injury, sterile inflammation and degeneration. Endogenous TLR ligands are called as damage-associated molecular patters (DAMPs), including endogenous molecules released by activated and necrotic cells, and extracellular matrix molecules. DAMPs are also known as alarmins. TLR research has brought about new insights in the rheumatic diseases. Previous reports suggest that TLRs and the signal pathways intensively contribute to the pathogenesis of rheumatoid arthritis (RA) and other arthritic conditions with interaction of various TLR ligands. Accumulated knowledge of TLR system is summarized to overlook TLRs and the signaling pathway in arthritis conditions, with special reference to RA.

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