依赖于M细胞的开始性摄取赋予Peyer贴片中的γδT17细胞的脑生现象型
Seiga Komiyama1,2, Yotaro Kodaira1, Rae Maeda3
1Division of Biochemistry, Faculty of Pharmacy and Graduate School of Pharmaceutical Sciences, Keio University, Tokyo 105-8512, Japan.
概括
产生互白素-17的 γδT17细胞是自身免疫性疾病的关键. 皮耶尔的共生细菌吸收.
科学领域:
- 免疫学 免疫学 免疫学
- 神经科学是一个神经科学.
- 微生物学 微生物学
背景情况:
- 产生互白素-17的 γδT 细胞 (γδT17 细胞) 在免疫调节中具有双重作用.
- 这些细胞在组织中起着保护作用,但在多发性硬化症等自身免疫性疾病中也会导致炎症.
- 参与γδT17细胞驱动自身免疫的特定机制和细胞类型,特别是中枢神经系统 (CNS) 中的细胞,尚未完全理解.
研究的目的:
- 阐明脑原性 γδT17 细胞的本体学和目录.
- 调查共生细菌和皮耶补丁微细胞 (M细胞) 在γδT17细胞激活和中枢神经系统炎症中的作用.
- 确定负责在实验性自身免疫脑膜炎 (EAE) 中启动炎症的特定 γδT17 细胞子集.
主要方法:
- 在实验性自身免疫脑膜炎 (EAE) 的背景下对 γδT17 细胞群的分析.
- 在皮耶尔贴片中研究微细胞 (M细胞) 依存的细菌吸收.
- 特定细菌物种的识别 (例如,乳杆菌种类). 和T细胞受体 (TCR) 刺激参与γδT17细胞激活.
主要成果:
- γδT17细胞的脑致性是由M细胞在皮耶尔斑块中吸收起生细菌的介导.
- 特定的共生细菌,如Lactobacillus spp.,通过TCR刺激激活CXCR6hiVγ6+Vδ1+不变的γδT17细胞.
- 在EAE早期阶段,γδT17细胞透到中枢神经系统,引发17型炎症.
结论:
- 皮耶补丁M细胞在将共生细菌与中枢神经系统炎症的发作联系起来的过程中至关重要.
- 这项研究确定了一种特定的途径,涉及自体免疫脑膜炎的病变发生过程中的共生细菌,M细胞和γδT17细胞.
- 这些发现凸显了自身免疫神经疾病中肠-大脑轴的关键机制.
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