J immunol:T-bet调节B细胞抵抗慢性病毒感染

2016-07-25 佚名 生物谷

在HIV,HBV,HCV,结核杆菌,疟原虫等等病原微生物的感染过程中,尽管宿主能够产生相应的免疫反应,但仍然无法阻止它们的持续性感染,原因在于这些免疫反应大多处于失活或衰竭的状态,无法清除所有的病原体。然而,在慢性感染过程中引发的免疫反应能够对病原体产生较高的压力,这一效应至少会打破病原体与宿主的动态博弈,从而延缓疾病的恶化过程。研究表明,体液免疫在病毒的持续性感染中具有重要的作用。事实上,尽管H

在HIV,HBV,HCV,结核杆菌,疟原虫等等病原微生物的感染过程中,尽管宿主能够产生相应的免疫反应,但仍然无法阻止它们的持续性感染,原因在于这些免疫反应大多处于失活或衰竭的状态,无法清除所有的病原体。然而,在慢性感染过程中引发的免疫反应能够对病原体产生较高的压力,这一效应至少会打破病原体与宿主的动态博弈,从而延缓疾病的恶化过程。

研究表明,体液免疫在病毒的持续性感染中具有重要的作用。事实上,尽管HIV能够通过突变的方式逃脱抗体的识别,但一些患者体内仍然能够自然产生广谱性中和抗体并有效抑制病毒的感染。不过,其中的作用机制目前并不清楚。之前的研究通过利用两种不同亚型的LCMV毒株对小鼠进行感染,结果显示:Cl13毒株在感染几个月后仍有部分的残余,在局部组织中有一定的复制活性;相反地,Arm毒株则在感染8-10天后就被宿主快速地清除。通过进一步比较,研究者们发现Cl13毒株相比Arm毒株在感染过程中能够更加有效抑制淋巴细胞的活性,但Cl13之所以没有造成系统性的感染,原因在于其体内B细胞的存在。当B细胞被敲除之后,宿主对Cl13的感染就变得难以控制。

为了研究B淋巴细胞在控制病毒慢性感染中的作用,来自美国宾夕法尼亚大学医学院的E. John Wherry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,作者比较了野生型与B细胞特异性Tbet缺失突变体小鼠在病毒感染过程中的差异。结果显示,突变体小鼠相比野生型其IgG2a的表达水平有明显下降,同时,小鼠对病毒的清除能力也有明显的缺陷。这一结果表明,B细胞中的T-bet以及其表达的IgG2a对于抵抗病毒慢性感染具有重要的作用。

进一步,作者对野生型小鼠与突变体小鼠进行了LCMV的急性感染。与上述结果不同,在急性感染过程中,T-bet的存在与否与小鼠对病毒的清除能力之间并没有明显的相关性。

之后,作者比较了在病毒慢性感染过程中T-bet调控的基因的表达谱特征。结果显示,T-bet调控了多类基因的表达,包括细胞迁移、增殖、抗体糖基化等等。这些基因的表达量的上调促进了抗病毒B细胞的活性以及抗病毒Ab的表达。

综上,作者证明B细胞中的T-bet的正常表达对于宿主抵抗病毒慢性感染具有重要的意义。

原始出处

Burton E. Barnett, Ryan P. Staupe, Pamela M. Odorizzi, Olesya Palko, Vesselin T. Tomov, Alison E. Mahan, Bronwyn Gunn, Diana Chen, Michael A. Paley, Galit Alter, Steven L. Reiner, Georg M. Lauer, John R. Teijaro and E. John Wherry.Cutting Edge: B Cell-Intrinsic T-bet Expression Is Required To Control Chronic Viral Infection.J immunol.2016

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    2016-08-20 yuanming7
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    2016-07-27 qjddjq
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    2016-07-25 1dd8c52fm63(暂无匿称)

    学习一下!

    0

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    2016-07-25 小屈86bae79a

    很高大上的研究成果

    0

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