Yu Shengyou, Qi Ren, Xiao Liang, Huang YiHui, Yu Li
Department of Pediatrics, Guangzhou First People's Hospital, South China University of Technology, Guangzhou, Guangdong, China.
Department of Rheumatology and Immunology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, Guangdong, China.
Front Immunol. 2025 Apr 30;16:1577109. doi: 10.3389/fimmu.2025.1577109. eCollection 2025.
Pediatric gout is a condition that differs from traditional adult gout and has attracted significant attention. This study aims to explore the molecular mechanisms underlying pediatric gout.
We analyzed peripheral blood samples from pediatric gout patients and healthy controls using single-cell RNA sequencing (scRNA-seq). Statistical tests were employed to analyze the data and identify significant differences between the groups.
Our findings revealed that CD14+ monocytes and DN T cells play crucial roles in pediatric gout. CD14+ monocytes are essential for recognizing and phagocytosing monosodium urate (MSU) crystals, triggering inflammation. DN T cells may be involved in the adaptive immune response within gouty joints. These cells not only contribute to the inflammatory response but also interact with other immune cells, amplifying the inflammatory cascade. Comparative analysis with adult gout studies highlighted both similarities and differences in cellular and molecular mechanisms between children and adults. The CD14+ monocytes may be interact with other immune cells through the TNF-α/NF-κB signaling pathway. Targeting this pathway may offer therapeutic potential for managing pediatric gout.
The results provide a foundation for new diagnostic markers and therapeutic targets for pediatric gout. They also pave the way for future research and the development of targeted therapies that can effectively manage and potentially prevent the debilitating effects of gout in children. Understanding the unique molecular mechanisms in pediatric gout could influence treatment strategies and improve patient outcomes.
儿童痛风是一种与传统成人痛风不同的病症，已引起广泛关注。本研究旨在探讨儿童痛风背后的分子机制。
我们使用单细胞RNA测序（scRNA-seq）分析了儿童痛风患者和健康对照的外周血样本。采用统计检验分析数据并确定组间的显著差异。
我们的研究结果表明，CD14+单核细胞和双阴性T细胞（DN T细胞）在儿童痛风中起关键作用。CD14+单核细胞对于识别和吞噬尿酸钠（MSU）晶体、引发炎症至关重要。DN T细胞可能参与痛风性关节内的适应性免疫反应。这些细胞不仅有助于炎症反应，还与其他免疫细胞相互作用，放大炎症级联反应。与成人痛风研究的比较分析突出了儿童和成人在细胞和分子机制上的异同。CD14+单核细胞可能通过肿瘤坏死因子-α/核因子-κB（TNF-α/NF-κB）信号通路与其他免疫细胞相互作用。针对该信号通路可能为儿童痛风的治疗提供潜在的治疗方法。
这些结果为儿童痛风的新诊断标志物和治疗靶点提供了基础。它们还为未来的研究以及靶向治疗的开发铺平了道路，这些靶向治疗可以有效地管理并可能预防痛风对儿童的致残影响。了解儿童痛风独特的分子机制可能会影响治疗策略并改善患者预后。
