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病毒通过细胞毒性T细胞依赖性破坏抗原呈递细胞和淋巴滤泡结构引发获得性免疫缺陷。

Virus-triggered acquired immunodeficiency by cytotoxic T-cell-dependent destruction of antigen-presenting cells and lymph follicle structure.

作者信息

Odermatt B, Eppler M, Leist T P, Hengartner H, Zinkernagel R M

机构信息

Institute of Pathology, University of Zürich, Switzerland.

出版信息

Proc Natl Acad Sci U S A. 1991 Sep 15;88(18):8252-6. doi: 10.1073/pnas.88.18.8252.

Abstract

Virus-induced acquired immune suppression in mice infected with lymphocytic choriomeningitis virus is shown here to be caused by the CD8+-T-cell-dependent elimination of macrophages/antigen-presenting cells. Surprisingly, this is associated with severe destruction of the follicular organization of lymphoid organs, indicating a crucial role for dendritic cells and marginal zone macrophages in maintaining follicular structure. Once established, this immunopathology cannot be readily reversed by the elimination of CD8+ effector cells. Such a T-cell-mediated pathogenesis may play a pivotal role in acquired virus-induced immunosuppression and may represent one strategy by which virus escapes immune surveillance and establishes persistent infections in initially immunocompetent hosts.

摘要

本文显示,感染淋巴细胞性脉络丛脑膜炎病毒的小鼠中,病毒诱导的获得性免疫抑制是由CD8 + T细胞依赖性消除巨噬细胞/抗原呈递细胞所致。令人惊讶的是,这与淋巴器官滤泡组织的严重破坏有关,表明树突状细胞和边缘区巨噬细胞在维持滤泡结构中起关键作用。一旦形成,这种免疫病理学不能通过消除CD8 +效应细胞轻易逆转。这种T细胞介导的发病机制可能在获得性病毒诱导的免疫抑制中起关键作用,并且可能代表病毒逃避免疫监视并在最初具有免疫能力的宿主中建立持续感染的一种策略。

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