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Published on: January 13, 2016
托尔类受体触发了维生素D介导的人类抗微生物反应
Philip T Liu1, Steffen Stenger, Huiying Li
1Department of Microbiology, Immunology, and Molecular Genetics, University of California at Los Angeles, Los Angeles, CA 90095, USA.
概括
人类巨细胞中的托尔类受体 (TLR) 激活增强了维生素D,增强了抗微生物甲基西西丁来对抗Mycobacterium tuberculosis. 在某些人群中,较低的维生素D水平与增加的结核病易感性相关.
科学领域:
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
- 营养科学 营养科学
背景情况:
- 收费类受体 (TLRs) 激活了对细胞内细菌的天生的免疫力.
- 氧化调解了TLR诱导的抗菌活性在小鼠,但不是人类的巨细胞.
- 维生素D在人类对Mycobacterium结核病的天生的免疫力中的作用仍在调查中.
研究的目的:
- 研究人类巨细胞中TLR诱导的抗微生物活性机制.
- 探索维生素D在TLR介导的对Mycobacterium结核病的天生的免疫力中的作用.
- 为了检查维生素D水平,cathelicidin诱导和结核病易感性之间的关联.
主要方法:
- 人类巨细胞中托尔类受体 (TLR) 的激活.
- 测量维生素D受体和维生素D-1-氧酶基因表达.
- 评估凯瑟利西丁诱导和杀死Mycobacterium结核病的作用.
- 在人类血清中分析25-氧维生素D水平和cathelicidin信使RNA诱导.
主要成果:
- 在人类巨细胞中,TLR激活上调调维生素D受体和维生素D-1-基酶基因表达.
- 这导致了抗微生物cathelicidin的诱导,并增强了细胞内Mycobacterium结核病菌的杀死.
- 低25-基维生素D水平和低效的cathelicidin信使RNA诱导在非洲裔美国人的血清中观察到,这些人患结核病的易感性增加了.
结论:
- 托尔类受体 (TLR) 和维生素D介导的先天免疫之间存在联系.
- 维生素D在人类巨细胞对Mycobacterium tuberculosis的反应中起着至关重要的作用.
- 人群中维生素D生产的变化可能会影响对结核病等微生物感染的易感性.
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