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Alpha-lactose reverses liver injury via blockade of Tim-3-mediated CD8 apoptosis in sepsis
Clinical Immunology ( IF 8.6 ) Pub Date : 2018-04-22 , DOI: 10.1016/j.clim.2018.04.010
Zhengping Wei , Pingfei Li , Yao Yao , Hai Deng , Shengwu Yi , Cong Zhang , Han Wu , Xiuxiu Xie , Minghui Xia , Ran He , Xiang-Ping Yang , Zhao-Hui Tang

In sepsis, the liver plays a crucial role in regulating immune responses and is also a target organ for immune-related injury. Despite the critical function of CD8+ T cells against opportunistic viral infections, the CD8 immune response in the liver during sepsis remains elusive. Here we found that Tim-3 is highly up-regulated in liver CD8+ T cells in a mouse cecal ligation and puncture model and in peripheral blood CD8+ T cells of human patients with sepsis. The expression of Tim-3 in liver CD8+ T cells displayed a bi-phasic pattern and deletion of Tim-3 led to reduction of CD8+ T cell apoptosis. Administration of α-lactose, a molecule with a similar structure to galactin-9, reduced Tim-3 expression and liver injury in sepsis. Our results demonstrate that targeting Tim-3 to boost CD8+ T cell immune response may offer an improved outcome in patients with sepsis.



中文翻译:

α-乳糖通过阻断脓毒症中Tim-3介导的CD8细胞凋亡逆转肝脏损伤

在脓毒症中,肝脏在调节免疫反应中起着至关重要的作用,也是免疫相关损伤的靶器官。尽管CD8 + T细胞具有抵抗机会性病毒感染的关键功能,但败血症期间肝脏中的CD8免疫反应仍然难以捉摸。在这里,我们发现,在小鼠盲肠结扎和穿刺模型中,Tim-3在肝CD8 + T细胞中以及在患有败血症的人类患者的外周血CD8 + T细胞中高度上调。肝CD8 + T细胞中Tim-3的表达呈双相模式,Tim-3的缺失导致CD8 +的减少。T细胞凋亡。α-乳糖(一种具有与半乳糖9相似的结构的分子)的给药可减少脓毒症中Tim-3的表达和肝损伤。我们的结果表明,靶向Tim-3来增强CD8 + T细胞免疫反应可能会改善败血症患者的预后。

更新日期:2018-04-22
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