白塞病葡萄膜炎（BDU）是一种慢性复发性自身免疫性疾病，病因复杂，治疗棘手，致盲率高。目前，CD4+T细胞功能紊乱是BDU重要致病机制之一，但上游机制尚未明确。NLRP3炎症小体/IL-1β和IL-18通路在自身免疫性疾病中起重要作用。临床上，IL-1β抑制剂可缓解BDU患者症状。NLRP3炎症小体/IL-18可能是BDU的另一重要致病机制，并可能与CD4+T细胞分化相关。我们前期发现，BDU活动期患者血清和尿液中Cathepsin B水平显著高于静止期。Cathepsin B是调控NLRP3炎症小体活性的上游分子。因此猜想：Cathepsin B通过激活NLRP3炎症小体/IL-18通路，影响CD4+T细胞分化，参与BDU发病。本研究以BDU患者外周血单个核细胞和实验性自身免疫性葡萄膜炎大鼠为研究对象，探索该通路在BDU中作用，寻找其潜在治疗靶点。

Behcet's disease uveitis (BDU) is a chronic recurrent autoimmune disease with complex causes, refractory disease courses, and high blinding rate. At present, CD4+T cell dysfunction is one of the important pathogenic mechanisms, but the upstream mechanism has not yet been clarified. The NLRP3 inflammasome/IL-1β and IL-18 pathways play important roles in a variety of chronic inflammation and autoimmune diseases. IL-1β is closely related to BDU, and inhibitors have good clinical effects. IL-18 downstream of the NLRP3 inflammasome may be another important pathogenic molecule of BDU, and may be related to CD4+T cell differentiation and polarization. We found that the levels of cathepsin B in serum and urine in patients with active BDU were significantly higher than those in resting phase. Cathepsin B is one of the upstream molecules that regulate the NLRP3 inflammasome activity. Therefore, it is speculated that cathepsin B may participate in the pathogenesis of BDU by activating the NLRP3 inflammasome/IL-18 pathway, and then affecting the differentiation of CD4+T cells. In this study, peripheral blood mononuclear cells (PBMC) from BDU patients and experimental autoimmune uveitis (EAU) rats were investigated. The role of this pathway in BDU was explored to find potential therapeutic targets.