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介素-1受体关联激酶-3的甲基化和多发性硬化症复发/活动的风险

Mona M Watany¹, Marwa M Elhosary², Hemat E El-Horany³

¹Clinical pathology department, Faculty of Medicine, Tanta University, Tanta 31527, Egypt.

Clinical immunology (Orlando, Fla.)

|July 25, 2024

概括

甲基化沉默介质素-1受体关联激酶-3 (IRAK-3) 与多发性硬化症 (MS) 的活性有关. 较高的IRAK-3甲基化预测MS复发风险,这表明它是一个潜在的生物标志物.

科学领域:

神经免疫学神经免疫学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
生物标志物发现发现

背景情况:

多发性硬化症 (MS) 是中枢神经系统的慢性炎症性脱髓化疾病.
表观遗传修饰,如DNA甲基化,与自身免疫性疾病的发病有关.
介素-1受体关联激酶-3 (IRAK-3/IRAK-M) 在免疫调节中发挥作用,其通过甲基化沉默在这里被研究.

研究的目的:

调查IRAK-3甲基化与多发性硬化症 (MS) 疾病活动之间的关联.
评估IRAK-3甲基化作为预测MS复发的潜在生物标志物.
探索IRAK-3甲基化,IRAK-3mRNA表达,MyD88和MS患者NF-κB活性之间的关系.

主要方法:

追溯横截面研究涉及90名参与者:45名患有活跃多发性硬化症,45名患有缓解期多发性硬化症和45名健康对照.
量化IRAK-3甲基化指数 (MI%),IRAK-3mRNA水平,循环骨髓分化因子88 (MyD88) 和核因子-卡帕B (NF-κB) 活性.
统计分析包括相关联和后勤回归建模,以评估预测值.

主要成果:

与缓解期患者相比,在活跃的MS患者中,IRAK-3MI%显著升高.
较高的IRAK-3MI%与较低的IRAK-3mRNA表达相关,MyD88增加,NF-κB活性增加.
结合IRAK-3甲基化的后勤回归模型显示了活性脱髓化强大的预测能力 (C指数=0.924).

结论:

伊拉克-3甲基化与活跃的多发性硬化症有显著的关联.
伊拉克-3甲基化作为一个有希望的候选生物标志物,用于识别患有复发风险的多发性硬化症患者.
通过调节MyD88/NF-κB通路,IRAK-3的表观遗传沉默可能有助于MS的发病.

关键词:

活动性脱髓化.伊拉克 - 伊拉克 - 伊拉克 - 伊拉克介素-1受体关联激酶-3 (IRAK-3) 的作用.多发性硬化症是多发性硬化症.骨髓分化的初级反应88 (MyD88)激活B细胞的核因子卡帕光链增强剂 (NF-κB)复发复发的情况

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