Chen Junwei, Wu Meng, Yang Jinhua, Wang Jing, Qiao Yue, Li Xiaofeng
Department of Rheumatology, Shanxi Medical University Second Affiliated Hospital, Shanxi, Taiyuan, 030001, China.
Iran J Immunol. 2017 Jun;14(2):90-98.
Gout is an inflammatory arthritis characterized by red, tender, hot and tumid joints. The development cause and process of gout is very sophisticated; recent studies, notwithstanding, have offered novel perspectives on the mechanism from an immunological viewpoint. The pathological process of gout involves both innate and adaptive immune responses. Other studies have demonstrated that gout development is associated with the presence of monosodium urate (MSU) crystals which serve as a "danger signal" affecting certain immune cells, cytokine production, and effector molecule expression, triggering both types of immune responses. Different cell subsets, cytokines, pattern recognition receptors (PRRs) and the inflammasome have had noticeable effects on the pathogenesis of gout. In the present review, we discuss the contributions of MSU-mediated immune responses in gout, which helps to better understand the mechanism of gout development.
痛风是一种炎症性关节炎，其特征为关节发红、触痛、发热和肿胀。痛风的发病原因和过程非常复杂；尽管如此，最近的研究从免疫学角度为其发病机制提供了新的观点。痛风的病理过程涉及先天性和适应性免疫反应。其他研究表明，痛风的发展与尿酸钠（MSU）晶体的存在有关，这些晶体作为一种“危险信号”，影响某些免疫细胞、细胞因子的产生和效应分子的表达，从而触发两种类型的免疫反应。不同的细胞亚群、细胞因子、模式识别受体（PRR）和炎性小体对痛风的发病机制产生了显著影响。在本综述中，我们讨论了MSU介导的免疫反应在痛风中的作用，这有助于更好地理解痛风的发病机制。
