活跃的权衡和低代谢状态促进疾病耐受性
Kirthana Ganeshan1, Joni Nikkanen1, Kevin Man1
1Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA 94143, USA.
Cell
|March 12, 2019
概括
免疫反应会引发能量损失,导致低新陈代谢和低温. 这种免疫诱导的低代谢促进了疾病耐受性,并且可能已经演变为组织耐受性机制.
科学领域:
- 免疫学
- 代谢研究
- 生态免疫学
背景情况:
- 宿主对病原体的防御是非常昂贵的.
- 免疫的代谢成本和它的权衡是鲜为人知的.
- 生态免疫学表明免疫力可能与其他维护功能交换.
研究的目的:
- 研究与免疫激活相关的能量权衡.
- 确定免疫诱导的能量成本的生理后果.
- 探索这些权衡对疾病耐受性的机制和影响.
主要方法:
- 激活免疫力和监测生理变化.
- 通过托尔类受体4 (TLR4) 途径分析对脂聚糖 (LPS) 的造血检测.
- 代谢学和全基因组表达特征以确定代谢程序.
主要成果:
- 免疫激活导致与同热的能量权衡,导致低代谢和低温.
- 这种权衡是独立的疾病行为,但需要收费类受体4 (TLR4) 信号.
- 不同的代谢程序调节进入和从低代谢状态恢复.
结论:
- 免疫诱导的低代谢节约能量,并在感染期间促进疾病耐受性.
- 像低代谢这样的节能状态可能已经演变为组织耐受性的机制.
- 研究结果显示免疫力,新陈代谢和疾病生存之间存在关键联系.
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