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EB病毒的天然免疫识别

Innate Immune Recognition of EBV.

作者信息

Lünemann Anna, Rowe Martin, Nadal David

机构信息

Division of Infectious Diseases and Hospital Epidemiology, University Children's Hospital of Zurich, Steinwiesstrasse 75, 8032, Zurich, Switzerland.

Children's Research Center, University Children's Hospital of Zurich, Zurich, Switzerland.

出版信息

Curr Top Microbiol Immunol. 2015;391:265-87. doi: 10.1007/978-3-319-22834-1_9.

DOI:10.1007/978-3-319-22834-1_9
PMID:26428378
Abstract

The ability of Epstein-Barr virus (EBV) to establish latency despite specific immune responses and to successfully persist lifelong in the human host shows that EBV has developed powerful strategies and mechanisms to exploit, evade, abolish, or downsize otherwise effective immune responses to ensure its own survival. This chapter focuses on current knowledge on innate immune responses against EBV and its evasion strategies for own benefit and summarizes the questions that remain to be tackled. Innate immune reactions against EBV originate both from the main target cells of EBV and from nontarget cells, which are elements of the innate immune system. Thus, we structured our review accordingly but with a particular focus on the innate recognition of EBV in its two stages in its life cycle, latent state and lytic replication. Specifically, we discuss (I) innate sensing and resulting innate immune responses against EBV by its main target cells, focusing on (i) EBV transmission between epithelial cells and B cells and their life cycle stages; and (ii) elements of innate immunity in EBV's target cells. Further, we debate (II) the innate recognition and resulting innate immune responses against EBV by cells other than the main target cells, focusing on (iii) myeloid cells: dendritic cells, monocytes, macrophages, and neutrophil granulocytes; and (iv) natural killer cells. Finally, we address (III) how EBV counteracts or exploits innate immunity in its latent and lytic life cycle stages, concentrating on (v) TLRs; (vi) EBERs; and (vii) microRNAs.

摘要

尽管存在特异性免疫反应,爱泼斯坦-巴尔病毒(EBV)仍能建立潜伏感染并在人类宿主中成功终身持续存在,这表明EBV已形成强大的策略和机制来利用、逃避、消除或削弱原本有效的免疫反应,以确保自身存活。本章重点介绍目前关于针对EBV的固有免疫反应及其自身获益的逃避策略的知识,并总结仍有待解决的问题。针对EBV的固有免疫反应既源于EBV的主要靶细胞,也源于作为固有免疫系统组成部分的非靶细胞。因此,我们相应地构建了本综述,但特别关注EBV在其生命周期的两个阶段,即潜伏状态和裂解复制阶段的固有识别。具体而言,我们讨论(I)其主要靶细胞对EBV的固有感知及由此产生的固有免疫反应,重点关注(i)上皮细胞与B细胞之间的EBV传播及其生命周期阶段;以及(ii)EBV靶细胞中的固有免疫成分。此外,我们探讨(II)主要靶细胞以外的细胞对EBV的固有识别及由此产生的固有免疫反应,重点关注(iii)髓样细胞:树突状细胞、单核细胞、巨噬细胞和中性粒细胞;以及(iv)自然杀伤细胞。最后,我们阐述(III)EBV如何在其潜伏和裂解生命周期阶段对抗或利用固有免疫,重点关注(v)Toll样受体(TLRs);(vi)EBV编码的小RNA(EBERs);以及(vii)微小RNA。

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