J immunol：IL-4, IL-21, 与IFN-γ共同调节激活B细胞T-bet基因表达

2016-07-21 佚名生物谷

尽管T-bet最初被发现作用了CD4 T细胞的分化，但它也同样参与了多种免疫细胞的转录调节活动。在慢性病毒感染中，B细胞内部的T-bet的能够促进其产生IgG2a，从而抑制病毒的感染。另外，T-bet也参与了与年龄相关的B细胞的产生，这部分B细胞与常规B细胞不同，但对病毒的清除以及自体体液免疫反应同样重要。最后，大部分T-bet阳性的B细胞都表达CD11c，这一表型特征标志着机体存在病毒、细菌或其

尽管T-bet最初被发现作用了CD4 T细胞的分化，但它也同样参与了多种免疫细胞的转录调节活动。在慢性病毒感染中，B细胞内部的T-bet的能够促进其产生IgG2a，从而抑制病毒的感染。另外，T-bet也参与了与年龄相关的B细胞的产生，这部分B细胞与常规B细胞不同，但对病毒的清除以及自体体液免疫反应同样重要。最后，大部分T-bet阳性的B细胞都表达CD11c，这一表型特征标志着机体存在病毒、细菌或其它病原体的感染。

尽管越来越多的证据表明T-bet阳性B细胞的生理作用，但这一亚群细胞的产生机制，以及其生理功能的调节过程都不太清楚。此前研究表明后天或先天的免疫受体，包括BCR以及TLR以及来自Tfh细胞的信号等都参与了T-bet阳性B细胞的分化与效应。具体地，IL-12、IL-18、IFN-g等都能够引起活化B细胞中T-bet转录因子的表达。不过，这些因子调节T-bet表达的胞内信号通路仍然没有完全揭示。

针对这一问题，来自美国宾夕法尼亚大学医学院的Michael P. Cancro课题组进行了深入研究，相关结果发表在最近一期的《Journal of Immunology》杂志上。

首先，作者通过体外刺激B细胞表面的TLR9受体，并给予IL-21的刺激，结果显示，IL-21能够进一步上调受到TL-9刺激后的B细胞中的T-bet基因的表达。进一步，作者发现IFN-g也具有上述效果，但IL-4则能够抑制IL-21引起的T-bet的表达。为了研究IL-21与IL-4是否直接调节了B细胞中T-bet的表达，作者将野生型B细胞与IL21r-/-或Stat-/-B细胞进行共同孵育。其中IL21R是IL-21的受体，而STAT6则是IL-4信号通路中的关键元件。作者希望了解这种共同孵育的操作能否产生一些细胞间的传递效应。结果显示，虽然IL-21能够促进野生型B细胞中T-bet的表达，而共同培养物中的突变体B细胞则始终呈T-bet阴性。这一结果表明IL-21信号直接调节了T-bet的活化。同样的，作者也证明了IL-4的抑制作用也是直接作用于IL-21信号本身。

进一步，作者通过体内试验验证了上述三种细胞因子能够调节胞内T-bet阳性、CD11c阳性的B细胞的形成，而IL-21促进CD11c的表达并不依赖于T-bet的活化。在流感病毒感染过程中，由于B细胞中的天然免疫受体被病毒抗原激活，即使缺少IFN-g，机体也能够产生T-bet、CD11c双阳性的B细胞，尽管此时常规B细胞的数量有明显的缺陷。

综上，作者证明了IL-4与IL-21协同作用调节了T-bet、CD11c双阳性B细胞的产生，这一过程并不依赖于IFN-g。

原始出处

Martin S. Naradikian, Arpita Myles, Daniel P. Beiting, Kenneth J. Roberts, Lucas Dawson, Ramin Sedaghat Herati, Bertram Bengsch, Susanne L. Linderman, Erietta Stelekati, Rosanne Spolski#, E. John Wherry, Christopher Hunter, Scott E. Hensley, Warren J. Leonard and Michael P. Cancro.Cutting Edge: IL-4, IL-21, and IFN-γ Interact To Govern T-bet and CD11c Expression in TLR-Activated B Cells.J immunol.2016

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#插入话题

插入图片

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2017-03-02 baoya

#IL-21#

39 0
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2016-09-04 ms5439512287675881

#BET#

24 0
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2016-11-08 yuanming7

#T-bet#

42 0
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2016-07-23 xiaoyeshuang

#B细胞#

23 0
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2016-07-23 bioon1

#基因表达#

33 0
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2016-07-23 bugit

#IFN#

36 0
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2016-07-23 tomyang93

#IL-2#

29 0

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