Cutting Edge: B Cell-Intrinsic T-bet Expression Is Required To Control Chronic Viral Infection.
Cutting Edge: B Cell-Intrinsic T-bet Expression Is Required To Control Chronic Viral Infection.
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尖端：B细胞中心T-bet表达需要控制慢性病毒感染。
DOI：
10.4049/jimmunol.1500368
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发表时间：
2016-08-15
期刊：
影响因子：
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通讯作者：
Wherry EJ
中科院分区：
文献类型：
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作者：
Barnett BE;Staupe RP;Odorizzi PM;Palko O;Tomov VT;Mahan AE;Gunn B;Chen D;Paley MA;Alter G;Reiner SL;Lauer GM;Teijaro JR;Wherry EJ
确立了抗体和B细胞在预防感染中的作用。相反，B细胞反应在控制慢性感染中的作用仍然知之甚少。IgG 2a（人类中的IgG 1）可以预防急性感染，T-bet促进IgG 2a同种型转换。然而，IgG 2a和B细胞表达的T-bet在持续感染期间是否影响宿主-病原体平衡尚不清楚。在这里，我们证明了B细胞特异性T-bet的丢失阻止了对持续病毒感染的控制。B细胞中的T-bet不仅控制IgG 2a的产生，而且控制粘膜定位、增殖、糖基化和广泛的转录程序。T-bet控制除IgG 2a之外的广泛抗病毒程序，因为即使在病毒特异性IgG 2a存在下，B细胞中的T-bet也是重要的。我们的数据支持一个模型，其中T-bet是跨多个免疫谱系的抗病毒免疫的通用控制器。
The role of antibody and B cells in preventing infection is established. In contrast, the role of B cell responses in containing chronic infections remains poorly understood. IgG2a (IgG1 in humans) can prevent acute infections and T-bet promotes IgG2a isotype switching. However, whether IgG2a and B cell-expressed T-bet influence the host-pathogen balance during persisting infections is unclear. Here we demonstrate that B cell specific loss of T-bet prevents control of persisting viral infection. T-bet in B cells not only controlled IgG2a production, but also mucosal localization, proliferation, glycosylation, and a broad transcriptional program. T-bet controlled a broad antiviral program in addition to IgG2a since T-bet in B cells was important even in the presence of virus-specific IgG2a. Our data supports a model in which T-bet is a universal controller of antiviral immunity across multiple immune lineages.