Antiviral immunity within neural stem cells distinguishes Enterovirus-D68 strain differences in forebrain organoids.

IF 9.3 1区 医学 Q1 IMMUNOLOGY Journal of Neuroinflammation Pub Date : 2024-11-05 DOI:10.1186/s12974-024-03275-5
Christine Vazquez, Seble G Negatu, Carl D Bannerman, Sowmya Sriram, Guo-Li Ming, Kellie A Jurado
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Abstract

Neural stem cells have intact innate immune responses that protect them from virus infection and cell death. Yet, viruses can antagonize such responses to establish neuropathogenesis. Using a forebrain organoid model system at two developmental time points, we identified that neural stem cells, in particular radial glia, are basally primed to respond to virus infection by upregulating several antiviral interferon-stimulated genes. Infection of these organoids with a neuropathogenic Enterovirus-D68 strain, demonstrated the ability of this virus to impede immune activation by blocking interferon responses. Together, our data highlight immune gene signatures present in different types of neural stem cells and differential viral capacity to block neural-specific immune induction.

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神经干细胞内的抗病毒免疫可区分前脑器官组织中的肠病毒-D68 株系差异。
神经干细胞具有完整的先天性免疫反应,可保护其免受病毒感染和细胞死亡。然而,病毒可以拮抗这种反应,从而建立神经发病机制。我们利用两个发育时间点的前脑类器官模型系统,发现神经干细胞,尤其是放射状胶质细胞,通过上调几个抗病毒干扰素刺激基因,对病毒感染做出基本反应。用神经致病性肠道病毒-D68株感染这些器官组织,证明这种病毒能够通过阻断干扰素反应来阻碍免疫激活。总之,我们的数据强调了不同类型神经干细胞中的免疫基因特征,以及不同病毒阻断神经特异性免疫诱导的能力。
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来源期刊
Journal of Neuroinflammation
Journal of Neuroinflammation 医学-神经科学
CiteScore
15.90
自引率
3.20%
发文量
276
审稿时长
1 months
期刊介绍: The Journal of Neuroinflammation is a peer-reviewed, open access publication that emphasizes the interaction between the immune system, particularly the innate immune system, and the nervous system. It covers various aspects, including the involvement of CNS immune mediators like microglia and astrocytes, the cytokines and chemokines they produce, and the influence of peripheral neuro-immune interactions, T cells, monocytes, complement proteins, acute phase proteins, oxidative injury, and related molecular processes. Neuroinflammation is a rapidly expanding field that has significantly enhanced our knowledge of chronic neurological diseases. It attracts researchers from diverse disciplines such as pathology, biochemistry, molecular biology, genetics, clinical medicine, and epidemiology. Substantial contributions to this field have been made through studies involving populations, patients, postmortem tissues, animal models, and in vitro systems. The Journal of Neuroinflammation consolidates research that centers around common pathogenic processes. It serves as a platform for integrative reviews and commentaries in this field.
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