前沿：控制慢性病毒感染需要B细胞内源性T-bet表达。
Cutting Edge: B Cell-Intrinsic T-bet Expression Is Required To Control Chronic Viral Infection.
作者信息
Barnett Burton E, Staupe Ryan P, Odorizzi Pamela M, Palko Olesya, Tomov Vesselin T, Mahan Alison E, Gunn Bronwyn, Chen Diana, Paley Michael A, Alter Galit, Reiner Steven L, Lauer Georg M, Teijaro John R, Wherry E John
机构信息
Department of Microbiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104; Institute for Immunology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104;
Institute for Immunology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104; Division of Gastroenterology, Department of Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104;
出版信息
J Immunol. 2016 Aug 15;197(4):1017-22. doi: 10.4049/jimmunol.1500368. Epub 2016 Jul 18.
The role of Ab 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. We demonstrate that B cell-specific loss of T-bet prevents control of persisting viral infection. T-bet in B cells controlled IgG2a production, as well as mucosal localization, proliferation, glycosylation, and a broad transcriptional program. T-bet controlled a broad antiviral program in addition to IgG2a because T-bet in B cells was important, even in the presence of virus-specific IgG2a. Our data support a model in which T-bet is a universal controller of antiviral immunity across multiple immune lineages.
抗体（Ab）和B细胞在预防感染中的作用已得到证实。相比之下，B细胞反应在控制慢性感染中的作用仍知之甚少。IgG2a（人类为IgG1）可预防急性感染，而T-bet促进IgG2a的同种型转换。然而，IgG2a和B细胞表达的T-bet在持续性感染期间是否影响宿主与病原体的平衡尚不清楚。我们证明，B细胞特异性缺失T-bet会阻碍对持续性病毒感染的控制。B细胞中的T-bet控制着IgG2a的产生，以及黏膜定位、增殖、糖基化和广泛的转录程序。除了IgG2a，T-bet还控制着广泛的抗病毒程序，因为即使存在病毒特异性IgG2a，B细胞中的T-bet也很重要。我们的数据支持这样一个模型，即T-bet是跨多个免疫谱系的抗病毒免疫的通用控制器。
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