T cell mediated suppression of neurotropic coronavirus replication in neural precursor cells

Neural precursor cells (NPCs) are the subject of intense investigation for their potential to treat neurodegenerative disorders, yet the consequences of neuroinvasive virus infection of NPCs remain unclear. This study demonstrates that NPCs support replication following infection by the neurotropic...

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Published in	Virology (New York, N.Y.) Vol. 449; pp. 235 - 243
Main Authors	Plaisted, Warren C., Weinger, Jason G., Walsh, Craig M., Lane, Thomas E.
Format	Journal Article
Language	English
Published	United States Elsevier Inc 20.01.2014
Subjects	Animals CD4-positive T-lymphocytes CD4-Positive T-Lymphocytes - immunology CD8-positive T-lymphocytes CD8-Positive T-Lymphocytes - immunology cell death Cells, Cultured Coronavirus Coronavirus Infections - immunology Coronavirus Infections - veterinary Coronavirus Infections - virology cytokines dose response Host response humans immunomodulation Infectious Disease interferon-gamma major histocompatibility complex Mice Mice, Inbred C57BL Murine hepatitis virus Murine hepatitis virus - genetics Murine hepatitis virus - physiology Neural precursor cells Neural Stem Cells - immunology Neural Stem Cells - virology neurodegenerative diseases Rodent Diseases - immunology Rodent Diseases - virology T cells Viral Tropism Virus Virus Replication viruses Virus Host response T cells Neural precursor cells
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Abstract	Neural precursor cells (NPCs) are the subject of intense investigation for their potential to treat neurodegenerative disorders, yet the consequences of neuroinvasive virus infection of NPCs remain unclear. This study demonstrates that NPCs support replication following infection by the neurotropic JHM strain of mouse hepatitis virus (JHMV). JHMV infection leads to increased cell death and dampens IFN-γ-induced MHC class II expression. Importantly, cytokines secreted by CD4+ T cells inhibit JHMV replication in NPCs, and CD8+ T cells specifically target viral peptide-pulsed NPCs for lysis. Furthermore, treatment with IFN-γ inhibits JHMV replication in a dose-dependent manner. Together, these findings suggest that T cells play a critical role in controlling replication of a neurotropic virus in NPCs, a finding which has important implications when considering immune modulation for NPC-based therapies for treatment of human neurologic diseases. •Murine neural precursor cells are infected by JHMV in a CEACAM1a-dependent manner.•Peptide-pulsed NPCs are targeted for lysis by virus-specific CD8+ T cells.•JHMV replication in NPCs is suppressed by CD4+ T cells through IFN-γ secretion.•IFN-γ dampens CEACAM1a expression and JHMV protein production in NPCs.
AbstractList	Neural precursor cells (NPCs) are the subject of intense investigation for their potential to treat neurodegenerative disorders, yet the consequences of neuroinvasive virus infection of NPCs remain unclear. This study demonstrates that NPCs support replication following infection by the neurotropic JHM strain of mouse hepatitis virus (JHMV). JHMV infection leads to increased cell death and dampens IFN-γ-induced MHC class II expression. Importantly, cytokines secreted by CD4+ T cells inhibit JHMV replication in NPCs, and CD8+ T cells specifically target viral peptide-pulsed NPCs for lysis. Furthermore, treatment with IFN-γ inhibits JHMV replication in a dose-dependent manner. Together, these findings suggest that T cells play a critical role in controlling replication of a neurotropic virus in NPCs, a finding which has important implications when considering immune modulation for NPC-based therapies for treatment of human neurologic diseases. Neural precursor cells (NPCs) are the subject of intense investigation for their potential to treat neurodegenerative disorders, yet the consequences of neuroinvasive virus infection of NPCs remain unclear. This study demonstrates that NPCs support replication following infection by the neurotropic JHM strain of mouse hepatitis virus (JHMV). JHMV infection leads to increased cell death and dampens IFN-γ-induced MHC class II expression. Importantly, cytokines secreted by CD4+ T cells inhibit JHMV replication in NPCs, and CD8+ T cells specifically target viral peptide-pulsed NPCs for lysis. Furthermore, treatment with IFN-γ inhibits JHMV replication in a dose-dependent manner. Together, these findings suggest that T cells play a critical role in controlling replication of a neurotropic virus in NPCs, a finding which has important implications when considering immune modulation for NPC-based therapies for treatment of human neurologic diseases. •Murine neural precursor cells are infected by JHMV in a CEACAM1a-dependent manner.•Peptide-pulsed NPCs are targeted for lysis by virus-specific CD8+ T cells.•JHMV replication in NPCs is suppressed by CD4+ T cells through IFN-γ secretion.•IFN-γ dampens CEACAM1a expression and JHMV protein production in NPCs. AbstractNeural precursor cells (NPCs) are the subject of intense investigation for their potential to treat neurodegenerative disorders, yet the consequences of neuroinvasive virus infection of NPCs remain unclear. This study demonstrates that NPCs support replication following infection by the neurotropic JHM strain of mouse hepatitis virus (JHMV). JHMV infection leads to increased cell death and dampens IFN-γ-induced MHC class II expression. Importantly, cytokines secreted by CD4+ T cells inhibit JHMV replication in NPCs, and CD8+ T cells specifically target viral peptide-pulsed NPCs for lysis. Furthermore, treatment with IFN-γ inhibits JHMV replication in a dose-dependent manner. Together, these findings suggest that T cells play a critical role in controlling replication of a neurotropic virus in NPCs, a finding which has important implications when considering immune modulation for NPC-based therapies for treatment of human neurologic diseases. Neural precursor cells (NPCs) are the subject of intense investigation for their potential to treat neurodegenerative disorders, yet the consequences of neuroinvasive virus infection of NPCs remain unclear. This study demonstrates that NPCs support replication following infection by the neurotropic JHM strain of mouse hepatitis virus (JHMV). JHMV infection leads to increased cell death and dampens IFN- gamma -induced MHC class II expression. Importantly, cytokines secreted by CD4+ T cells inhibit JHMV replication in NPCs, and CD8+ T cells specifically target viral peptide-pulsed NPCs for lysis. Furthermore, treatment with IFN- gamma inhibits JHMV replication in a dose-dependent manner. Together, these findings suggest that T cells play a critical role in controlling replication of a neurotropic virus in NPCs, a finding which has important implications when considering immune modulation for NPC-based therapies for treatment of human neurologic diseases. Neural precursor cells (NPCs) are the subject of intense investigation for their potential to treat neurodegenerative disorders, yet the consequences of neuroinvasive virus infection of NPCs remain unclear. This study demonstrates that NPCs support replication following infection by the neurotropic JHM strain of mouse hepatitis virus (JHMV). JHMV infection leads to increased cell death and dampens IFN-γ-induced MHC class II expression. Importantly, cytokines secreted by CD4+ T cells inhibit JHMV replication in NPCs, and CD8+ T cells specifically target viral peptide-pulsed NPCs for lysis. Furthermore, treatment with IFN-γ inhibits JHMV replication in a dose-dependent manner. Together, these findings suggest that T cells play a critical role in controlling replication of a neurotropic virus in NPCs, a finding which has important implications when considering immune modulation for NPC-based therapies for treatment of human neurologic diseases.Neural precursor cells (NPCs) are the subject of intense investigation for their potential to treat neurodegenerative disorders, yet the consequences of neuroinvasive virus infection of NPCs remain unclear. This study demonstrates that NPCs support replication following infection by the neurotropic JHM strain of mouse hepatitis virus (JHMV). JHMV infection leads to increased cell death and dampens IFN-γ-induced MHC class II expression. Importantly, cytokines secreted by CD4+ T cells inhibit JHMV replication in NPCs, and CD8+ T cells specifically target viral peptide-pulsed NPCs for lysis. Furthermore, treatment with IFN-γ inhibits JHMV replication in a dose-dependent manner. Together, these findings suggest that T cells play a critical role in controlling replication of a neurotropic virus in NPCs, a finding which has important implications when considering immune modulation for NPC-based therapies for treatment of human neurologic diseases. Neural precursor cells (NPCs) are the subject of intense investigation for their potential to treat neurodegenerative disorders, yet the consequences of neuroinvasive virus infection of NPCs remain unclear. This study demonstrates that NPCs support replication following infection by the neurotropic JHM strain of mouse hepatitis virus (JHMV). JHMV infection leads to increased cell death and dampens IFN-γ-induced MHC class II expression. Importantly, cytokines secreted by CD4+ T cells inhibit JHMV replication in NPCs, and CD8+ T cells specifically target viral peptide-pulsed NPCs for lysis. Furthermore, treatment with IFN-γ inhibits JHMV replication in a dose-dependent manner. Together, these findings suggest that T cells play a critical role in controlling replication of a neurotropic virus in NPCs, a finding which has important implications when considering immune modulation for NPC-based therapies for treatment of human neurologic diseases. • Murine neural precursor cells are infected by JHMV in a CEACAM1a-dependent manner. • Peptide-pulsed NPCs are targeted for lysis by virus-specific CD8+ T cells. • JHMV replication in NPCs is suppressed by CD4+ T cells through IFN-γ secretion. • IFN-γ dampens CEACAM1a expression and JHMV protein production in NPCs.
Author	Plaisted, Warren C. Walsh, Craig M. Weinger, Jason G. Lane, Thomas E.
Author_xml	– sequence: 1 givenname: Warren C. surname: Plaisted fullname: Plaisted, Warren C. organization: Department of Molecular Biology & Biochemistry, University of California, Irvine 92697-3900, USA – sequence: 2 givenname: Jason G. surname: Weinger fullname: Weinger, Jason G. organization: Department of Molecular Biology & Biochemistry, University of California, Irvine 92697-3900, USA – sequence: 3 givenname: Craig M. surname: Walsh fullname: Walsh, Craig M. organization: Department of Molecular Biology & Biochemistry, University of California, Irvine 92697-3900, USA – sequence: 4 givenname: Thomas E. surname: Lane fullname: Lane, Thomas E. email: tom.lane@path.utah.edu organization: Department of Molecular Biology & Biochemistry, University of California, Irvine 92697-3900, USA
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Keywords	Virus Host response T cells Neural precursor cells
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Snippet	Neural precursor cells (NPCs) are the subject of intense investigation for their potential to treat neurodegenerative disorders, yet the consequences of... AbstractNeural precursor cells (NPCs) are the subject of intense investigation for their potential to treat neurodegenerative disorders, yet the consequences...
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SubjectTerms	Animals CD4-positive T-lymphocytes CD4-Positive T-Lymphocytes - immunology CD8-positive T-lymphocytes CD8-Positive T-Lymphocytes - immunology cell death Cells, Cultured Coronavirus Coronavirus Infections - immunology Coronavirus Infections - veterinary Coronavirus Infections - virology cytokines dose response Host response humans immunomodulation Infectious Disease interferon-gamma major histocompatibility complex Mice Mice, Inbred C57BL Murine hepatitis virus Murine hepatitis virus - genetics Murine hepatitis virus - physiology Neural precursor cells Neural Stem Cells - immunology Neural Stem Cells - virology neurodegenerative diseases Rodent Diseases - immunology Rodent Diseases - virology T cells Viral Tropism Virus Virus Replication viruses
Title	T cell mediated suppression of neurotropic coronavirus replication in neural precursor cells
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