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Cell Death Dis:Nfkbie缺乏增加B淋巴细胞增生性疾病的易感性

2020-03-21 MedSci原创 MedSci原创

在细胞的存活、分化、增殖、炎症及免疫调节等多种过程中,NF-κB信号转导通路均起着重要的作用。而异常激活的NF-κB是大多数B细胞恶性肿瘤发生发展的标志。这种激活可能是由于与肿

在细胞的存活、分化、增殖、炎症及免疫调节等多种过程中,NF-κB信号转导通路均起着重要的作用。而异常激活的NF-κB是大多数B细胞恶性肿瘤发生发展的标志。这种激活可能是由于与肿瘤微环境的相互作用或体细胞突变影响NF-κB家族成员或其上游相关信号转导因子而引起的。

在慢性淋巴细胞性白血病和原发性纵隔B细胞淋巴瘤等发病频率较高的几种B细胞恶性肿瘤中经常能够观察到NFKBIE基因的失活,而该基因所编码的IκBε是一种NF-κB抑制剂,能够抑制其蛋白活性并参与NF-κB信号通路的活化过程。 然而NFKBIE的缺乏对于B细胞的发育及功能的影响目前仍然未知。

为了更深入地了解NFKBIE在正常及恶性B细胞分化中的作用,研究人员建立了Nfkbie缺失小鼠,并发现Nfkbie的缺乏能够导致边缘区B细胞及B1细胞亚群扩增。
 
在生发中心(GC)依赖性的免疫应答中,Nfkbie缺乏可以通过以B细胞自主性细胞增殖的方式引起GC中B细胞的扩增。Nfkbie的缺乏也会导致B1细胞亚群的过度增殖,并在Toll样受体刺激下引起这些细胞中活化的NF-κB的增加。
 
此外,Nfkbie的缺乏能够与突变的MYD88协同发挥作用,进而导致B细胞增殖能力的增强。在老年小鼠中,Nfkbie的缺乏会导致单克隆惰性B淋巴细胞增生性疾病的发生发展,这一表型类似于单克隆B淋巴细胞增多症。

总而言之,本研究结果阐明了IκBε在B细胞发育及功能中所起的重要的微调作用。

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    2020-11-28 docwu2019
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    2020-11-28 huagfeg
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  5. 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11:36:34 CST 2020, time=2020-03-23, status=1, ipAttribution=), GetPortalCommentsPageByObjectIdResponse(id=380855, encodeId=718d38085565, content=好, beContent=null, objectType=article, channel=null, level=null, likeNumber=108, replyNumber=0, topicName=null, topicId=null, topicList=[], attachment=null, authenticateStatus=null, createdAvatar=, createdBy=bbc11488193, createdName=thm112988, createdTime=Mon Mar 23 00:28:08 CST 2020, time=2020-03-23, status=1, ipAttribution=)]
  6. 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  7. 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  8. 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    2020-03-23 thm112988

    0

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