痛风
受体
TLR4型
TLR2型
细胞内
免疫学
Toll样受体
关节炎
细胞生物学
调解人
信号转导
炎症
生物
先天免疫系统
医学
遗传学
生物化学
作者
Cássia Regina Silva,André Lopes Saraiva,Mateus Rossato,Gabriela Trevisan,Sara Marchesan Oliveira
出处
期刊:Endocrine, metabolic & immune disorders
[Bentham Science]
日期:2022-05-26
卷期号:23 (4): 446-457
被引量:5
标识
DOI:10.2174/1871530322666220523145728
摘要
Abstract: 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 has 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 TLRs 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 evidence regarding the involvement of TLRs in gout arthritis pathogenesis, with particular reference to TLR2 and TLR4, by analyzing the actual literature data.
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