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早在一个世纪以前,加洛德医师指出尿酸盐的沉积是导致痛风的原因而不是结果,而Hollander等在痛风患者的关节滑液中检出单钠尿酸盐(MSU)晶体,进一步证实了MSU晶体是引起痛风的原因之一[1]。因此,MSU晶体的致炎机制受到了风湿和免疫学家的广泛关注。固有免疫系统在感染和损伤所介导的炎性反应中占主导作用,并且能快速启动宿主防御反应,趋化获得性免疫相关细胞移动至炎症部位而引起免疫应答。研究发现,MSU晶体可作为一种危险相关模式分子(DAMPs),通过与病原相关模式分子(PAMPs)相似的方式激
As early as a century ago, Dr. Garold pointed out that the deposition of urate was the cause of gout but not the result, and Hollander et al. Detected monosodium urate (MSU) crystals in the synovial fluid of gout patients, further confirming The MSU crystal is one of the causes of gout [1]. Therefore, the mechanism of inflammation of MSU crystals has attracted the attention of rheumatism and immunologists. The innate immune system plays a predominant role in the inflammatory response mediated by infection and injury and can rapidly initiate host defense responses that trigger the immune response by chemotactic immune-related cells moving to the site of inflammation. The study found that MSU crystals can act as a dangerous mode-of-the-mode (DAMPs) molecule, stimulated in a similar manner to pathogen-associated pattern molecules (PAMPs)