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在多发性硬化症中,加勒-3的转录上调

Katia Mangano¹, Maria Cristina Petralia², Rita Bella³

¹Department of Biomedical and Biotechnological Sciences, University of Catania, Via S. Sofia 89, 95123, Catania, Italy.

Immunologic research

|July 26, 2023

概括

在多发性硬化症 (MS) 发育过程中,免疫细胞和中枢神经系统细胞中,加勒-3的水平显著升高. 这一发现强调了加勒-3的存在.

科学领域:

神经免疫学神经免疫学
中枢神经系统 (CNS) 疾病
自免疫性疾病自免疫性疾病

背景情况:

多发性硬化症 (MS) 是一种中枢神经系统自身免疫性疾病,影响全球数以百万计的人,其致病性尚未完全理解.
galectins,特别是 galectin-3,涉及免疫调节和中枢神经系统平衡,这表明在MS中可能发挥作用.
神经炎症和神经退行是MS的关键特征,促使人们对诸如加勒-3等分子进行研究.

研究的目的:

综合分析多发性硬化症病原体中细胞组件中加勒-3表达的核心成分.
研究加勒-3与参与中枢神经系统内免疫和炎症反应的基因的共同表达模式.
确定加勒-3在多发性硬化症中的潜在病原遗传作用.

主要方法:

在MS的临床前模型 (MOG诱导的实验性过敏性脑膜炎 - EAE) 中对脑原 CD4 + T 细胞的 galectin-3 转录基因水平的评估.
分析EAE小鼠脊髓中分离的微质细胞,星体细胞和寡体细胞中的加列-3表达.
检查人类MS相关白质病变中的加勒-3水平.
模块化联合表达分析以识别与加勒-3相关的基因.

主要成果:

在EAE模型中,在脑性 CD4+ T 细胞中观察到显著更高的 galectin-3 转录基因水平.
从EAE小鼠脊髓中检测到微质细胞,星体细胞和小体细胞中显著增加的加勒-3水平.
在人类MS白质病变中也发现了加勒-3表达的增加.
加勒-3与调节微质细胞,细胞因子生产和化学反应的基因共同表达.

结论:

这项研究提供了在多发性硬化症的背景下对加列-3表达的第一个全面分析.
在各种中枢神经系统细胞类型和人类多发性硬化病变中,高高的加勒-3水平表明具有显著的病原遗传作用.
加列-3与免疫相关基因的共同表达加强了其参与MS背后的炎症过程.

关键词:

盖莱克-3 是一种盖莱克酸是一种质蛋白质.多发性硬化症是多发性硬化症.

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