Nicola Cotugno , Giulio Olivieri , Giuseppe Rubens Pascucci , Donato Amodio , Elena Morrocchi , Chiara Pighi , Emma Concetta Manno , Gioacchino Andrea Rotulo , Carolina D'Anna , Marcello Chinali , Isabella Tarissi de Jacobis , Danilo Buonsenso , Alberto Villani , Paolo Rossi , Alessandra Marchesi , Paolo Palma
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引用次数: 0
Abstract
Despite progress, the molecular mechanisms underlying Kawasaki Disease (KD) and intravenous immunoglobulin's (IVIG) ability to mitigate the inflammatory process remain poorly understood. To characterize this condition, plasma proteomic profiles, flow cytometry, and gene expression of T cell subsets were investigated in longitudinal samples from KD patients and compared with two control groups. Systems-level analysis of samples in the acute phase revealed distinctive inflammatory features of KD, involving mainly Th-1 and Th-17 mediators and unveiled a potential disease severity signature. APBB1IP demonstrated an association with coronary artery involvement (CAI) and was significantly higher in CAI+ compared to CAI- patients. Integrative analysis revealed a transient reduction in CD4+ EM T cells and a comprehensive immune activation and exhaustion. Following treatment, Tregs at both frequency and gene expression levels revealed immune dynamics of recovery. Overall, our data provide insights into KD, which may offer valuable information on prognostic indicators and possible targets for novel treatments.
尽管取得了进展,但人们对川崎病(KD)的分子机制以及静脉注射免疫球蛋白(IVIG)缓解炎症过程的能力仍然知之甚少。为了描述川崎病的特征,研究人员对川崎病患者的纵向样本进行了血浆蛋白质组图谱、流式细胞术和 T 细胞亚群基因表达的研究,并与两个对照组进行了比较。对急性期样本进行的系统级分析揭示了KD独特的炎症特征,主要涉及Th-1和Th-17介质,并揭示了潜在的疾病严重性特征。APBB1IP与冠状动脉受累(CAI)有关,在CAI+患者中明显高于CAI-患者。综合分析表明,CD4+ EM T细胞短暂减少,免疫系统全面激活和衰竭。治疗后,Tregs在频率和基因表达水平上都显示出免疫动态恢复。总之,我们的数据提供了对 KD 的见解,这可能会为预后指标和新型治疗的可能靶点提供有价值的信息。
期刊介绍:
Clinical Immunology publishes original research delving into the molecular and cellular foundations of immunological diseases. Additionally, the journal includes reviews covering timely subjects in basic immunology, along with case reports and letters to the editor.