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The dural innate immune barrier protects the CNS from systemic virus invasion

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE209575 | GEO | 2022/07/25

REPOSITORIES: GEO

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The dural innate immune barrier protects the CNS from systemic virus invasion [MHCII_10X]

Project description:To investigate heterogeneity of MHCII high CNS border-associated mononuclear phagocytes (BAMPs), MHCII high BAMPs from 30 adult male mice were FACS sorted and single-cell RNA seqs were performed

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The dural innate immune barrier protects the CNS from systemic virus invasion [EC_10X]

Project description:To investigate heterogeneity of CNS border vasculatures, endothelial cells (EC) from 30 adult male mice were FACS sorted and single-cell RNA seqs were performed

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The dural innate immune barrier protects the CNS from systemic virus invasion [CD45_10X]

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The dural innate immune barrier protects the CNS from systemic virus invasion

Project description:The dural innate immune barrier protects the CNS from systemic virus invasion

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The dural innate immune barrier protects the CNS from systemic virus invasion [CD45_10X]

Project description:The dural innate immune barrier protects the CNS from systemic virus invasion [CD45_10X]

| PRJNA861269 | ENA

The dural innate immune barrier protects the CNS from systemic virus invasion [MHCII_10X]

Project description:The dural innate immune barrier protects the CNS from systemic virus invasion [MHCII_10X]

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Susceptibilities of CNS Cells towards Rabies Virus Infection Is Linked to Cellular Innate Immune Responses.

Project description:Rabies is caused by neurotropic rabies virus (RABV), contributing to 60,000 human deaths annually. Even though rabies leads to major public health concerns worldwide, we still do not fully understand factors determining RABV tropism and why glial cells are unable to clear RABV from the infected brain. Here, we compare susceptibilities and immune responses of CNS cell types to infection with two RABV strains, Tha and its attenuated variant Th2P-4M, mutated on phospho- (P-protein) and matrix protein (M-protein). We demonstrate that RABV replicates in human stem cell-derived neurons and astrocytes but fails to infect human iPSC-derived microglia. Additionally, we observed major differences in transcription profiles and quantification of intracellular protein levels between antiviral immune responses mediated by neurons, astrocytes (IFNB1, CCL5, CXCL10, IL1B, IL6, and LIF), and microglia (CCL5, CXCL10, ISG15, MX1, and IL6) upon Tha infection. We also show that P- and M-proteins of Tha mediate evasion of NF-κB- and JAK-STAT-controlled antiviral host responses in neuronal cell types in contrast to glial cells, potentially explaining the strong neuron-specific tropism of RABV. Further, Tha-infected astrocytes and microglia protect neurons from Tha infection via a filtrable and transferable agent. Overall, our study provides novel insights into RABV tropism, showing the interest in studying the interplay of CNS cell types during RABV infection.

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