Busso N, Ea H-K
DAL, Service de Rhumatologie, Centre Hospitalier Universitaire Vaudois, University of Lausanne, Switzerland.
Reumatismo. 2012 Jan 19;63(4):230-7. doi: 10.4081/reumatismo.2011.230.
Recent advances have stimulated new interest in the area of crystal arthritis, as microcrystals can be considered to be endogenous "danger signals" and are potent stimulators of immune as well as non-immune cells. The best known microcrystals include urate (MSU), and calcium pyrophosphate (CPP) crystals, associated with gout and pseudogout, respectively. Acute inflammation is the hallmark of the acute tissue reaction to crystals in both gout and pseudogout. The mechanisms leading to joint inflammation in these diseases involve first crystal formation and subsequent coating with serum proteins. Crystals can then interact with plasma cell membrane, either directly or via membrane receptors, leading to NLRP3 activation, proteolytic cleavage and maturation of pro-interleukin-1β (pro-IL1β) and secretion of mature IL1β. Once released, this cytokine orchestrates a series of events leading to endothelial cell activation and neutrophil recruitment. Ultimately, gout resolution involves several mechanisms including monocyte differentiation into macrophage, clearance of apoptotic neutrophils by macrophages, production of Transforming Growth Factor (TGF-β) and modification of protein coating on the crystal surface. This review will examine these different steps.
最近的进展激发了人们对晶体性关节炎领域的新兴趣，因为微晶可被视为内源性“危险信号”，并且是免疫细胞和非免疫细胞的强效刺激物。最知名的微晶包括尿酸盐（MSU）和焦磷酸钙（CPP）晶体，分别与痛风和假性痛风相关。急性炎症是痛风和假性痛风中急性组织对晶体反应的标志。这些疾病中导致关节炎症的机制首先涉及晶体形成，随后晶体被血清蛋白包被。然后，晶体可直接或通过膜受体与浆细胞膜相互作用，导致NLRP3激活、前白细胞介素-1β（pro-IL1β）的蛋白水解切割和成熟，以及成熟IL1β的分泌。一旦释放，这种细胞因子会引发一系列导致内皮细胞激活和中性粒细胞募集的事件。最终，痛风的缓解涉及多种机制，包括单核细胞分化为巨噬细胞、巨噬细胞清除凋亡的中性粒细胞、转化生长因子（TGF-β）的产生以及晶体表面蛋白包被的改变。本综述将探讨这些不同的步骤。
