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Activation of type I interferon antiviral response in human neural stem cells
by
Kuo, Rei-Lin
, Lin, Jhao-Yin
, Huang, Hsing-I
in
Antiviral drugs
/ Biological response modifiers
/ Biomedical and Life Sciences
/ Biomedical Engineering and Bioengineering
/ Cell Biology
/ Cell Line
/ Cells, Cultured
/ Central nervous system
/ DEAD Box Protein 58 - genetics
/ DEAD Box Protein 58 - immunology
/ Encephalitis
/ Encephalitis Viruses, Japanese - immunology
/ Encephalitis, Japanese - genetics
/ Encephalitis, Japanese - immunology
/ Genes
/ Genomes
/ Humans
/ IFN
/ Immune response
/ Immunity, Innate
/ Infection
/ Infections
/ Innate immunity
/ Interferon
/ Interferon Lambda
/ Interferon Type I - biosynthesis
/ Interferon Type I - immunology
/ Interferon-beta - biosynthesis
/ Interferon-beta - genetics
/ Interferon-beta - immunology
/ Interferons - genetics
/ Interferons - immunology
/ Japanese encephalitis
/ Life Sciences
/ MDA5
/ Neural stem cells
/ Neural Stem Cells - immunology
/ Neural Stem Cells - pathology
/ Neural Stem Cells - virology
/ Neurogenesis
/ Neurological diseases
/ Pathogenic microorganisms
/ Pathogens
/ Pattern recognition receptors
/ Polyinosinic:polycytidylic acid
/ Receptors, Immunologic
/ Regenerative Medicine/Tissue Engineering
/ Ribonucleic acid
/ RIG-I
/ RNA
/ Sensors
/ Stem Cells
/ TLR3 protein
/ TLR7 protein
/ Toll-like receptors
/ Transcription activation
/ Transcription, Genetic
/ Transfection
/ Viral infections
/ Viruses
/ West Nile virus
/ Zika virus
/ Zika Virus - immunology
/ Zika Virus Infection - genetics
/ Zika Virus Infection - immunology
/ Zika Virus Infection - pathology
/ β-Interferon
2019
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Activation of type I interferon antiviral response in human neural stem cells
by
Kuo, Rei-Lin
, Lin, Jhao-Yin
, Huang, Hsing-I
in
Antiviral drugs
/ Biological response modifiers
/ Biomedical and Life Sciences
/ Biomedical Engineering and Bioengineering
/ Cell Biology
/ Cell Line
/ Cells, Cultured
/ Central nervous system
/ DEAD Box Protein 58 - genetics
/ DEAD Box Protein 58 - immunology
/ Encephalitis
/ Encephalitis Viruses, Japanese - immunology
/ Encephalitis, Japanese - genetics
/ Encephalitis, Japanese - immunology
/ Genes
/ Genomes
/ Humans
/ IFN
/ Immune response
/ Immunity, Innate
/ Infection
/ Infections
/ Innate immunity
/ Interferon
/ Interferon Lambda
/ Interferon Type I - biosynthesis
/ Interferon Type I - immunology
/ Interferon-beta - biosynthesis
/ Interferon-beta - genetics
/ Interferon-beta - immunology
/ Interferons - genetics
/ Interferons - immunology
/ Japanese encephalitis
/ Life Sciences
/ MDA5
/ Neural stem cells
/ Neural Stem Cells - immunology
/ Neural Stem Cells - pathology
/ Neural Stem Cells - virology
/ Neurogenesis
/ Neurological diseases
/ Pathogenic microorganisms
/ Pathogens
/ Pattern recognition receptors
/ Polyinosinic:polycytidylic acid
/ Receptors, Immunologic
/ Regenerative Medicine/Tissue Engineering
/ Ribonucleic acid
/ RIG-I
/ RNA
/ Sensors
/ Stem Cells
/ TLR3 protein
/ TLR7 protein
/ Toll-like receptors
/ Transcription activation
/ Transcription, Genetic
/ Transfection
/ Viral infections
/ Viruses
/ West Nile virus
/ Zika virus
/ Zika Virus - immunology
/ Zika Virus Infection - genetics
/ Zika Virus Infection - immunology
/ Zika Virus Infection - pathology
/ β-Interferon
2019
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Activation of type I interferon antiviral response in human neural stem cells
by
Kuo, Rei-Lin
, Lin, Jhao-Yin
, Huang, Hsing-I
in
Antiviral drugs
/ Biological response modifiers
/ Biomedical and Life Sciences
/ Biomedical Engineering and Bioengineering
/ Cell Biology
/ Cell Line
/ Cells, Cultured
/ Central nervous system
/ DEAD Box Protein 58 - genetics
/ DEAD Box Protein 58 - immunology
/ Encephalitis
/ Encephalitis Viruses, Japanese - immunology
/ Encephalitis, Japanese - genetics
/ Encephalitis, Japanese - immunology
/ Genes
/ Genomes
/ Humans
/ IFN
/ Immune response
/ Immunity, Innate
/ Infection
/ Infections
/ Innate immunity
/ Interferon
/ Interferon Lambda
/ Interferon Type I - biosynthesis
/ Interferon Type I - immunology
/ Interferon-beta - biosynthesis
/ Interferon-beta - genetics
/ Interferon-beta - immunology
/ Interferons - genetics
/ Interferons - immunology
/ Japanese encephalitis
/ Life Sciences
/ MDA5
/ Neural stem cells
/ Neural Stem Cells - immunology
/ Neural Stem Cells - pathology
/ Neural Stem Cells - virology
/ Neurogenesis
/ Neurological diseases
/ Pathogenic microorganisms
/ Pathogens
/ Pattern recognition receptors
/ Polyinosinic:polycytidylic acid
/ Receptors, Immunologic
/ Regenerative Medicine/Tissue Engineering
/ Ribonucleic acid
/ RIG-I
/ RNA
/ Sensors
/ Stem Cells
/ TLR3 protein
/ TLR7 protein
/ Toll-like receptors
/ Transcription activation
/ Transcription, Genetic
/ Transfection
/ Viral infections
/ Viruses
/ West Nile virus
/ Zika virus
/ Zika Virus - immunology
/ Zika Virus Infection - genetics
/ Zika Virus Infection - immunology
/ Zika Virus Infection - pathology
/ β-Interferon
2019
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Activation of type I interferon antiviral response in human neural stem cells
Journal Article
Activation of type I interferon antiviral response in human neural stem cells
2019
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Overview
Background
Neural stem cells (NSCs) residing in the central nervous system play an important role in neurogenesis. Several viruses can infect these neural progenitors and cause severe neurological diseases. The innate immune responses against the neurotropic viruses in these tissue-specific stem cells remain unclear.
Methods
Human NSCs were transfected with viral RNA mimics or infected with neurotropic virus for detecting the expression of antiviral interferons (IFNs) and downstream IFN-stimulated antiviral genes.
Results
NSCs are able to produce interferon-β (IFN-β) (type I) and λ1 (type III) after transfection with poly(I:C) and that downstream IFN-stimulated antiviral genes, such as ISG56 and MxA, and the viral RNA sensors RIG-I, MDA5, and TLR3, can be expressed in NSCs under poly(I:C) or IFN-β stimulation. In addition, our results show that the pattern recognition receptors RIG-I and MDA5, as well as the endosomal pathogen recognition receptor TLR3, but not TLR7 and TLR8, are involved in the activation of IFN-β transcription in NSCs. Furthermore, NSCs infected with the neurotropic viruses, Zika and Japanese encephalitis viruses, are able to induce RIG-I-mediated IFN-β expression.
Conclusion
Human NSCs have the ability to activate IFN signals against neurotropic viral pathogens.
Publisher
BioMed Central,BioMed Central Ltd,Springer Nature B.V,BMC
Subject
/ Biological response modifiers
/ Biomedical and Life Sciences
/ Biomedical Engineering and Bioengineering
/ DEAD Box Protein 58 - genetics
/ DEAD Box Protein 58 - immunology
/ Encephalitis Viruses, Japanese - immunology
/ Encephalitis, Japanese - genetics
/ Encephalitis, Japanese - immunology
/ Genes
/ Genomes
/ Humans
/ IFN
/ Interferon Type I - biosynthesis
/ Interferon Type I - immunology
/ Interferon-beta - biosynthesis
/ Interferon-beta - immunology
/ MDA5
/ Neural Stem Cells - immunology
/ Neural Stem Cells - pathology
/ Neural Stem Cells - virology
/ Pattern recognition receptors
/ Polyinosinic:polycytidylic acid
/ Regenerative Medicine/Tissue Engineering
/ RIG-I
/ RNA
/ Sensors
/ Viruses
/ Zika Virus Infection - genetics
/ Zika Virus Infection - immunology
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