乳酸脱酶-提升病毒感染抑制MOG呈现CD11b+CD11c+树突细胞在多发性硬化症的小鼠模型中
Pyone Pyone Soe1, Mélanie Gaignage1, Mohamed F Mandour1,2
1de Duve Institute, Universite Catholique de Louvain, 1200 Brussels, Belgium.
International journal of molecular sciences
|May 11, 2024
概括
乳酸脱酶升高病毒 (LDV) 感染可以预防实验性自身免疫脑膜炎 (EAE),这是多发性硬化症 (MS) 的一种模型. LDV减少了树突细胞的髓抗原的呈现,防止了自身免疫T细胞的激活.
科学领域:
- 神经免疫学 神经免疫学
- 病毒学 病毒学
- 免疫学 免疫学 免疫学
背景情况:
- 像多发性硬化症 (MS) 这样的自身免疫性中枢神经系统疾病可能受到感染的影响.
- 实验性自身免疫脑膜炎 (EAE) 是对MS的小鼠模型.
研究的目的:
- 研究乳酸脱酶升高病毒 (LDV) 感染对EAE发展的保护作用.
- 阐明LDV介导保护的潜在免疫机制.
主要方法:
- 在免疫接种前,小鼠感染了LDV,并用髓寡干细胞糖蛋白 (MOG35-55) 诱导EAE.
- 评估了疾病的严重程度,体重减轻和中枢神经系统组织病理学.
- 分析了树突细胞 (DC) 对T淋巴细胞的抗原呈现.
主要成果:
- 与未感染的对照组相比,LDV感染显著保护小鼠免受EAE,减少和体重减轻.
- 组织病理学检查显示,LDV感染小鼠中枢神经系统的脱髓化和炎症细胞透减少.
- LDV感染减少了由CD11b+CD11c+树突细胞向致病性T淋巴细胞的MOG的呈现.
结论:
- LDV感染通过抑制特定的树突细胞子集对自反应性T淋巴细胞的髓质抗原呈现来保护EAE.
- 这种机制可能解释了感染对自身免疫性疾病的更广泛的抑制作用,与卫生假说保持一致.
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