Abstract: Uric Acid (UA), a weak acid and the final metabolite of purine degradation, exists in two primary forms in vivo: soluble UA (sUA) and Monosodium Urate (MSU) crystals. It is predominantly excreted through urine after the catabolism of adenine and guanine, maintaining a dynamic equilibrium within physiological conditions. UA exhibits notable antioxidant properties that contribute to the maintenance of redox homeostasis and the modulation of immune responses. However, disruptions caused by diet, lifestyle, or metabolic abnormalities can disturb UA equilibrium, resulting in oxidative imbalance, immune dysregulation, and chronic inflammation. Autoimmune Diseases (ADs) arise from a breakdown of immune tolerance, leading to the activation of autoreactive T and B cells, excessive autoantibody formation, dysregulated cytokine networks, and sustained tissue-damaging inflammation. Emerging evidence has unveiled that UA may trigger and participate in the onset and progression of several types of ADs by initiating oxidative stress (OS), modulating immune responses, and amplifying inflammatory mediators. In this review, summarize current advances in understanding the immunological roles of UA in the initiation and progression of ADs. We also evaluate the clinical relevance of UA as an immunomodulatory biomarker and therapeutic target. Furthermore, we explore conventional therapeutic approaches for ADs in combination with UA-lowering interventions, aiming to identify optimized treatment strategies tailored to specific autoimmune conditions to improve clinical outcomes.
Gao et al. (2026) studied this question.