子[a]二烯暴露会导致异位切换,从而以AHR-依赖的方式减少表面CD5表达
Smita Kumari1, Bharat Singh1, Amit Kumar Kureel1
1Department of Biotechnology, Motilal Nehru National Institute of Technology Allahabad, Prayagraj, U.P. 211004, India.
Immunology letters
|April 17, 2024
概括
多环芳,如BaP,通过调节一个替代性外显子 (E1B) 来降低T细胞中的表面CD5 (sCD5) 表达. 这种由基碳化合物受体 (AHR) 介导的开关可能会损害T细胞功能.
科学领域:
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
- 环境健康 环境健康
背景情况:
- 在T细胞中CD5蛋白的表面表达是至关重要的,但尚未完全理解.
- CD5表面表达的变化与免疫病理学和血液恶性瘤有关.
- 来自人类内源逆转录病毒 (HERV) 的替代外基子 (E1B) 降低了传统的CD5 (E1A) 表达,导致细胞内保留 (cCD5).
研究的目的:
- 调查CD5替代外因子 (E1B) 表达的调节.
- 确定二氧化碳暴露和基碳化合物受体 (AHR) 在CD5调控中的作用.
- 通过CD5调制了解多环芳在T细胞功能上的影响.
主要方法:
- 在体转录因子结合部位 (TFBS) 分析E1B上游区域.
- 细胞暴露于甲 (BaP) 和E1A/E1B表达的分析.
- 染色体免疫沉定量PCR (ChIP-qPCR) 来确认AHR的结合性.
- AHR抑制和基因沉默研究.
主要成果:
- 在E1B上游地区确定了五种假定的二氧化物反应元素 (DREs).
- 暴露于BaP上调了E1B表达,同时降低了E1A表达和表面 (sCD5) 和细胞内 (cCD5) 蛋白质.
- ChIP-qPCR证实了AHR与预测的DRE站点的结合.
- 通过抑制剂和基因沉默实验证实了AHR参与外基因切换.
结论:
- 多环芳通过AHR上调替代性外显子E1B的表达,从而降低sCD5的表达.
- 这种机制涉及AHR介导的外部开关,可能会对T细胞功能产生负面影响.
- 这些发现突出了一个新的途径,将环境污染物与改变的免疫细胞功能联系起来.
关键词:
美国人权委员会 (AHR)CD5 CD5 CD5 CD5 CD5 CD5 CD5 CD5 CD5 CD5 CD5 CD5 CD5 CD5 CD5 CD5 CD5 CD5E1B E1B E1B E1B E1B E1B E1B E1B E1B E1B E1B E1B E1B E1B E1B E1B E1B E1B E1B E1B E1B E1B赫尔夫 (HERV) 公司一个T细胞细胞.更多相关视频
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