Suppr超能文献

疫苗诱导的 CD4 T 细胞可防止慢性感染中抗病毒 B 细胞的缺失。

Vaccine-elicited CD4 T cells prevent the deletion of antiviral B cells in chronic infection.

机构信息

Division of Experimental Virology, Department of Biomedicine, University of Basel, 4003 Basel, Switzerland.

Immune Cell Biology Laboratory, Department of Biomedicine, University Hospital Basel, 4031 Basel, Switzerland.

出版信息

Proc Natl Acad Sci U S A. 2021 Nov 16;118(46). doi: 10.1073/pnas.2108157118.

Abstract

Chronic viral infections subvert protective B cell immunity. An early type I interferon (IFN-I)-driven bias to short-lived plasmablast differentiation leads to clonal deletion, so-called "decimation," of antiviral memory B cells. Therefore, prophylactic countermeasures against decimation remain an unmet need. We show that vaccination-induced CD4 T cells prevented the decimation of naïve and memory B cells in chronically lymphocytic choriomeningitis virus (LCMV)-infected mice. Although these B cell responses were largely T independent when IFN-I was blocked, preexisting T help assured their sustainability under conditions of IFN-I-driven inflammation by instructing a germinal center B cell transcriptional program. Prevention of decimation depended on T cell-intrinsic Bcl6 and Tfh progeny formation. Antigen presentation by B cells, interactions with antigen-specific T helper cells, and costimulation by CD40 and ICOS were also required. Importantly, B cell-mediated virus control averted Th1-driven immunopathology in LCMV-challenged animals with preexisting CD4 T cell immunity. Our findings show that vaccination-induced Tfh cells represent a cornerstone of effective B cell immunity to chronic virus challenge, pointing the way toward more effective B cell-based vaccination against persistent viral diseases.

摘要

慢性病毒感染颠覆了保护性 B 细胞免疫。早期的 I 型干扰素(IFN-I)驱动的偏向短暂的浆母细胞分化导致抗病毒记忆 B 细胞的克隆性缺失,即所谓的“耗竭”。因此,预防耗竭仍然是一个未满足的需求。我们表明,疫苗接种诱导的 CD4 T 细胞可防止慢性淋巴细胞性脉络丛脑膜炎病毒(LCMV)感染小鼠中幼稚和记忆 B 细胞的耗竭。尽管在阻断 IFN-I 时,这些 B 细胞反应在很大程度上是 T 细胞非依赖性的,但预先存在的 T 辅助细胞通过指导生发中心 B 细胞转录程序,确保了它们在 IFN-I 驱动的炎症条件下的可持续性。预防耗竭取决于 T 细胞内在的 Bcl6 和 Tfh 前体形成。B 细胞的抗原呈递、与抗原特异性 T 辅助细胞的相互作用以及 CD40 和 ICOS 的共刺激也是必需的。重要的是,B 细胞介导的病毒控制避免了具有预先存在的 CD4 T 细胞免疫的 LCMV 挑战动物中的 Th1 驱动的免疫病理学。我们的研究结果表明,疫苗接种诱导的 Tfh 细胞是慢性病毒挑战中有效 B 细胞免疫的基石,为针对持续性病毒病的更有效的基于 B 细胞的疫苗接种指明了方向。

相似文献

本文引用的文献

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验