抗原特异性B细胞受体使B细胞对流感病毒感染敏感
Stephanie K Dougan1, Joseph Ashour, Roos A Karssemeijer
11] Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, Massachusetts 02142, USA [2].
Nature
|October 22, 2013
概括
流感A病毒专门感染并杀死识别其血凝素的B细胞. 这种在肺部向的B细胞破坏延迟了保护性抗体的产生,帮助病毒感染.
科学领域:
- 免疫学 免疫学 免疫学
- 病毒学 病毒学
- 分子生物学分子生物学
背景情况:
- B 淋巴细胞及其抗体对抗甲型流感病毒的保护至关重要.
- 流感病毒与流感特异性B细胞相互作用并影响流感病毒的确切机制尚不完全理解.
研究的目的:
- 为了研究流感血素特异性B细胞和流感A病毒之间的相互作用的结果.
- 阐明B细胞受体 (BCR) 在病毒诱导的B细胞感染和死亡中的作用.
主要方法:
- 通过体细胞核转移,生成含有流感A/WSN/33病毒血质素特异性BCRB细胞的FluBI小鼠.
- 分析病毒结合,B细胞感染,抗体分泌和与流感A病毒相互作用时的B细胞死亡.
- 在感染小鼠的体内研究中,评估肺部和淋巴结居住的FluBI B细胞的命运.
主要成果:
- 流感A/WSN/33病毒特别感染血凝素特异性B细胞 (FluBI细胞),但不控制B细胞,尽管通过酸结合等效的病毒.
- 对于B细胞感染,BCR与病毒血凝素的相互作用是必不可少的,导致抗体分泌中断和B细胞在18小时内死亡.
- 在受感染的小鼠中,肺部居住的FluBI B细胞被感染并死亡,延迟了保护性抗体的释放,而淋巴结居住的FluBI B细胞没有被感染并繁殖.
结论:
- 流感病毒积极向并消除肺环境中的病毒特异性B细胞.
- 这种免疫规避策略允许病毒在有效的自适应性免疫反应之前建立感染.
- 了解这种机制可以了解病毒病原和潜在的治疗点.
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