Papers of the Week

Toll-like receptors (TLRs) are a well-characterized family of cell-bound pattern recognition receptors able to identify and respond to conserved structures of external microorganisms or Pathogen Molecular-Associated Pattern (PAMPs). They can also interact with Damage-Associated Molecular Patterns (DAMPs) involved with any infectious and sterile cell stress of tissue injury. Accumulated knowledge about TLRs had revealed that these receptors and intracellular signaling pathways triggered through TLR activation contribute to the physiopathology of different inflammatory diseases, including arthritic conditions. Mostly, the literature focuses on exploring TLR in rheumatoid and osteoarthritis, however, TLRs also seem to be an essential mediator for monosodium urate (MSU) crystals induced gouty arthritis, both in animal models and humans. Accordingly, naked MSU crystals have a highly negatively charged surface recognized by TLRs; intracellular adapter protein MyD88 are significant mediators of MSU crystals-induced IL1β production in mice, and gouty patients demonstrate a robust positive correlation between TLR4 mRNA level and serum IL1β. Here, we revised the literature pieces of evidence surrounding the involvement of TLRs in gout arthritis pathogenesis, with particular reference to TLR2 and TLR4, by analyzing the actual literature data.