由人类B淋巴细胞产生的氧化抑制了细胞亡和爱斯坦-巴尔病毒的重新激活
J B Mannick1, K Asano, K Izumi
1Department of Microbiology and Molecular Genetics, Harvard Medical School, Brigham and Women's Hospital, Boston, Massachusetts 02115.
Cell
|December 30, 1994
概括
氧化 (NO) 在人体B细胞中构成性表达,在抑制亡和维持爱斯坦-巴尔病毒 (EBV) 潜伏性方面发挥关键作用. 这一发现澄清了NO的NO.
科学领域:
- 免疫学 免疫学 免疫学
- 病毒学 病毒学
- 细胞生物学 细胞生物学
背景情况:
- 氧化 (NO) 对小鼠对病毒感染的抗性至关重要.
- 人类免疫反应中NO的作用,特别是单核细胞中的作用,仍然不清楚.
- 爱斯坦-巴尔病毒 (EBV) 感染人体B淋巴细胞,建立潜伏期.
研究的目的:
- 研究人类B淋巴细胞中氧化合成酶 (NOS) 的表达和功能.
- 确定NO在EBV潜伏期和B细胞亡中的作用.
主要方法:
- 在EBV转化B淋巴细胞和伯基特淋巴瘤细胞系中评估诱导性氧化合成酶 (iNOS) 表达.
- 研究了NO对EBV交换主体Zta表达的作用.
- 研究了NO对亡和cGMP独立信号通路的影响.
主要成果:
- 在人类B淋巴细胞细胞系中检测到构成性,低水平的iNOS表达.
- 发现NO的产生降低了Zta表达的调节,保持了EBV的延迟.
- NO在B淋巴细胞细胞系中抑制了亡,独立于cGMP.
结论:
- NO在人类B细胞生物学中起着生理作用.
- NO有助于抑制B细胞中编程细胞死亡.
- 在人类B细胞中,NO参与维持病毒延迟,特别是EBV.
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