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  1. Article ; Online: Tracking Plasmacytoid Dendritic Cell Response to Physical Contact with Infected Cells.

    Ribeiro, Margarida Sá / Joshi, Garima / Décembre, Elodie / Nuovo, Célia / Bosseboeuf, Adrien / Bellomo, Alicia / Venet, Manon / Assil, Sonia / Dreux, Marlène

    Methods in molecular biology (Clifton, N.J.)

    2023  Volume 2618, Page(s) 289–315

    Abstract: Dendritic cells (DCs) are key regulators of both innate and adaptive immunity via varied functions, including cytokine production and antigen presentation. Plasmacytoid DC (pDC) is a DC subset specialized in the production of type I and III interferons ( ... ...

    Abstract Dendritic cells (DCs) are key regulators of both innate and adaptive immunity via varied functions, including cytokine production and antigen presentation. Plasmacytoid DC (pDC) is a DC subset specialized in the production of type I and III interferons (IFNs). They are thus pivotal players of the host antiviral response during the acute phase of infection by genetically distant viruses. The pDC response is primarily triggered by the endolysosomal sensors Toll-like receptors, which recognize nucleic acids from pathogens. In some pathologic contexts, pDC response can also be triggered by host nucleic acids, hereby contributing to the pathogenesis of autoimmune diseases, such as, e.g., systemic lupus erythematosus. Importantly, recent in vitro studies from our laboratory and others uncovered that pDCs sense viral infections when a physical contact is established with infected cells. This specialized synapse-like feature enables a robust type I and III IFN secretion at the infected site. Therefore, this concentrated and confined response likely limits the correlated deleterious impacts of excessive cytokine production to the host, notably due to tissue damages. Here we provide a pipeline of methods for ex vivo studies of pDC antiviral functions, designed to address how pDC activation is regulated by cell-cell contact with virally infected cells and the current approaches enabling to decipher the underlying molecular events leading to an efficient antiviral response.
    MeSH term(s) Immunity, Innate ; Antiviral Agents ; Interferons ; Dendritic Cells ; Nucleic Acids ; Interferon Type I/metabolism
    Chemical Substances Antiviral Agents ; Interferons (9008-11-1) ; Nucleic Acids ; Interferon Type I
    Language English
    Publishing date 2023-03-11
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-2938-3_21
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Interplay between SARS-CoV-2 and the type I interferon response.

    Sa Ribero, Margarida / Jouvenet, Nolwenn / Dreux, Marlène / Nisole, Sébastien

    PLoS pathogens

    2020  Volume 16, Issue 7, Page(s) e1008737

    Abstract: The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is responsible for the current COVID-19 pandemic. An unbalanced immune response, characterized by a weak production of type I interferons (IFN-Is) and an exacerbated release of ... ...

    Abstract The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is responsible for the current COVID-19 pandemic. An unbalanced immune response, characterized by a weak production of type I interferons (IFN-Is) and an exacerbated release of proinflammatory cytokines, contributes to the severe forms of the disease. SARS-CoV-2 is genetically related to SARS-CoV and Middle East respiratory syndrome-related coronavirus (MERS-CoV), which caused outbreaks in 2003 and 2013, respectively. Although IFN treatment gave some encouraging results against SARS-CoV and MERS-CoV in animal models, its potential as a therapeutic against COVID-19 awaits validation. Here, we describe our current knowledge of the complex interplay between SARS-CoV-2 infection and the IFN system, highlighting some of the gaps that need to be filled for a better understanding of the underlying molecular mechanisms. In addition to the conserved IFN evasion strategies that are likely shared with SARS-CoV and MERS-CoV, novel counteraction mechanisms are being discovered in SARS-CoV-2-infected cells. Since the last coronavirus epidemic, we have made considerable progress in understanding the IFN-I response, including its spatiotemporal regulation and the prominent role of plasmacytoid dendritic cells (pDCs), which are the main IFN-I-producing cells. While awaiting the results of the many clinical trials that are evaluating the efficacy of IFN-I alone or in combination with antiviral molecules, we discuss the potential benefits of a well-timed IFN-I treatment and propose strategies to boost pDC-mediated IFN responses during the early stages of viral infection.
    MeSH term(s) Antiviral Agents/therapeutic use ; Betacoronavirus/drug effects ; Betacoronavirus/immunology ; Betacoronavirus/isolation & purification ; COVID-19 ; Coronavirus Infections/drug therapy ; Coronavirus Infections/immunology ; Coronavirus Infections/virology ; Dendritic Cells/drug effects ; Dendritic Cells/immunology ; Humans ; Immunity, Innate/drug effects ; Immunity, Innate/immunology ; Interferon Type I/therapeutic use ; Pandemics ; Pneumonia, Viral/drug therapy ; Pneumonia, Viral/immunology ; Pneumonia, Viral/virology ; Prognosis ; SARS-CoV-2 ; COVID-19 Drug Treatment
    Chemical Substances Antiviral Agents ; Interferon Type I
    Keywords covid19
    Language English
    Publishing date 2020-07-29
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2205412-1
    ISSN 1553-7374 ; 1553-7374
    ISSN (online) 1553-7374
    ISSN 1553-7374
    DOI 10.1371/journal.ppat.1008737
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Interplay between SARS-CoV-2 and the type I interferon response.

    Margarida Sa Ribero / Nolwenn Jouvenet / Marlène Dreux / Sébastien Nisole

    PLoS Pathogens, Vol 16, Iss 7, p e

    2020  Volume 1008737

    Abstract: The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is responsible for the current COVID-19 pandemic. An unbalanced immune response, characterized by a weak production of type I interferons (IFN-Is) and an exacerbated release of ... ...

    Abstract The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is responsible for the current COVID-19 pandemic. An unbalanced immune response, characterized by a weak production of type I interferons (IFN-Is) and an exacerbated release of proinflammatory cytokines, contributes to the severe forms of the disease. SARS-CoV-2 is genetically related to SARS-CoV and Middle East respiratory syndrome-related coronavirus (MERS-CoV), which caused outbreaks in 2003 and 2013, respectively. Although IFN treatment gave some encouraging results against SARS-CoV and MERS-CoV in animal models, its potential as a therapeutic against COVID-19 awaits validation. Here, we describe our current knowledge of the complex interplay between SARS-CoV-2 infection and the IFN system, highlighting some of the gaps that need to be filled for a better understanding of the underlying molecular mechanisms. In addition to the conserved IFN evasion strategies that are likely shared with SARS-CoV and MERS-CoV, novel counteraction mechanisms are being discovered in SARS-CoV-2-infected cells. Since the last coronavirus epidemic, we have made considerable progress in understanding the IFN-I response, including its spatiotemporal regulation and the prominent role of plasmacytoid dendritic cells (pDCs), which are the main IFN-I-producing cells. While awaiting the results of the many clinical trials that are evaluating the efficacy of IFN-I alone or in combination with antiviral molecules, we discuss the potential benefits of a well-timed IFN-I treatment and propose strategies to boost pDC-mediated IFN responses during the early stages of viral infection.
    Keywords Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5 ; covid19
    Subject code 610
    Language English
    Publishing date 2020-07-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Monitoring of Interferon Response Triggered by Cells Infected by Hepatitis C Virus or Other Viruses Upon Cell-Cell Contact.

    Coléon, Séverin / Assil, Sonia / Dreux, Marlène

    Methods in molecular biology (Clifton, N.J.)

    2018  Volume 1911, Page(s) 319–335

    Abstract: Plasmacytoid dendritic cells (pDCs) constitute a unique DC subset specialized in rapid and massive secretion of cytokines, including type I interferon (i.e., IFNα and IFNβ), known to be pivotal for both innate immunity and the onset of adaptive response. ...

    Abstract Plasmacytoid dendritic cells (pDCs) constitute a unique DC subset specialized in rapid and massive secretion of cytokines, including type I interferon (i.e., IFNα and IFNβ), known to be pivotal for both innate immunity and the onset of adaptive response. The production of type I IFNs by pDCs is primarily induced by the recognition of viral nucleic acids through Toll-like receptor (TLR)-7 and -9 sensors located in the endolysosomal compartment. Importantly, in the context of hepatitis C virus (HCV) infection, pDC type I IFN response is triggered by the sensing of infected cells via physical cell-cell contact. Such a feature is also observed for many genetically distant viruses, including notably viruses of the Retroviridae, Arenaviridae, Flaviviridae, Picornaviridaea, Togaviridae families and observed for various infected cell types. Here, we described a set of experimental methods for the ex vivo studies of the regulation of pDC activation upon physical cell-cell contact with virally infected cells.
    MeSH term(s) Cell Line ; Cells, Cultured ; Coculture Techniques/methods ; Dendritic Cells/immunology ; Enzyme-Linked Immunosorbent Assay/methods ; Flow Cytometry/methods ; Hepacivirus/immunology ; Hepatitis C/immunology ; Humans ; Immunity, Innate ; In Situ Hybridization, Fluorescence/methods ; Interferon Type I/immunology ; Microscopy, Confocal/methods ; Microscopy, Fluorescence/methods ; Toll-Like Receptors/immunology
    Chemical Substances Interferon Type I ; Toll-Like Receptors
    Language English
    Publishing date 2018-12-27
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-4939-8976-8_22
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: HCV transmission by hepatic exosomes establishes a productive infection.

    Cosset, François-Loïc / Dreux, Marlène

    Journal of hepatology

    2014  Volume 60, Issue 3, Page(s) 674–675

    MeSH term(s) Exosomes/virology ; Hepacivirus/genetics ; Humans ; RNA, Viral/genetics ; Virion/genetics
    Chemical Substances RNA, Viral
    Language English
    Publishing date 2014-03
    Publishing country Netherlands
    Document type Comment ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 605953-3
    ISSN 1600-0641 ; 0168-8278
    ISSN (online) 1600-0641
    ISSN 0168-8278
    DOI 10.1016/j.jhep.2013.10.015
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: La susceptibilité à l'infection par le virus de l'hépatite C et la réponse antivirale sont modulées par le polymorphisme associé à l'interféron lambda.

    Assil, Sonia / Dreux, Marlène

    Medecine sciences : M/S

    2014  Volume 30, Issue 12, Page(s) 1073–1075

    Title translation Modulation of permissiveness and antiviral response against hepatitis C virus by interferon lambda-associated polymorphism.
    MeSH term(s) Antiviral Agents ; Genetic Predisposition to Disease/genetics ; Hepatitis C/immunology ; Humans ; Interferons/genetics ; Polymorphism, Genetic
    Chemical Substances Antiviral Agents ; Interferons (9008-11-1)
    Language French
    Publishing date 2014-12
    Publishing country France
    Document type News
    ZDB-ID 632733-3
    ISSN 1958-5381 ; 0767-0974
    ISSN (online) 1958-5381
    ISSN 0767-0974
    DOI 10.1051/medsci/20143012006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Interplay between SARS-CoV-2 and the type I interferon response

    Sa Ribero, Margarida / Jouvenet, Nolwenn / Dreux, Marlène / Nisole, Sébastien

    PLOS Pathogens

    2020  Volume 16, Issue 7, Page(s) e1008737

    Keywords Immunology ; Genetics ; Molecular Biology ; Microbiology ; Parasitology ; Virology ; covid19
    Language English
    Publisher Public Library of Science (PLoS)
    Publishing country us
    Document type Article ; Online
    ZDB-ID 2205412-1
    ISSN 1553-7374 ; 1553-7366
    ISSN (online) 1553-7374
    ISSN 1553-7366
    DOI 10.1371/journal.ppat.1008737
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: Cell-Cell Sensing of Viral Infection by Plasmacytoid Dendritic Cells.

    Webster, Brian / Assil, Sonia / Dreux, Marlène

    Journal of virology

    2016  Volume 90, Issue 22, Page(s) 10050–10053

    Abstract: All cells possess signaling pathways designed to trigger antiviral responses, notably characterized by type I interferon (IFN) production, upon recognition of invading viruses. Especially, host sensors recognize viral nucleic acids. Nonetheless, ... ...

    Abstract All cells possess signaling pathways designed to trigger antiviral responses, notably characterized by type I interferon (IFN) production, upon recognition of invading viruses. Especially, host sensors recognize viral nucleic acids. Nonetheless, virtually all viruses have evolved potent strategies that preclude host responses within the infected cells. The plasmacytoid dendritic cell (pDC) is an immune cell type known as a robust type I IFN producer in response to viral infection. Evidence suggests that such functionality of the pDCs participates in viral clearance. Nonetheless, their contribution, which is likely complex and varies depending on the pathogen, is still enigmatic for many viruses. pDCs are not permissive to most viral infections, and consistently, recent examples suggest that pDCs respond to immunostimulatory viral RNA transferred via noninfectious and/or noncanonical viral/cellular carriers. Therefore, the pDC response likely bypasses innate signaling blockages induced by virus within infected cells. Importantly, the requirement for cell-cell contact is increasingly recognized as a hallmark of the pDC-mediated antiviral state, triggered by evolutionarily divergent RNA viruses.
    MeSH term(s) Animals ; Cytokines/immunology ; Dendritic Cells/immunology ; Humans ; Immunity, Innate/immunology ; Interferon Type I/immunology ; Signal Transduction/immunology ; Virus Diseases/immunology
    Chemical Substances Cytokines ; Interferon Type I
    Language English
    Publishing date 2016-10-28
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 80174-4
    ISSN 1098-5514 ; 0022-538X
    ISSN (online) 1098-5514
    ISSN 0022-538X
    DOI 10.1128/JVI.01692-16
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Interplay between SARS-CoV-2 and the type I interferon response

    Sa Ribero, Margarida / Jouvenet, Nolwenn / Dreux, Marlène / Nisole, Sébastien

    PLoS Pathog

    Abstract: The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is responsible for the current COVID-19 pandemic. An unbalanced immune response, characterized by a weak production of type I interferons (IFN-Is) and an exacerbated release of ... ...

    Abstract The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is responsible for the current COVID-19 pandemic. An unbalanced immune response, characterized by a weak production of type I interferons (IFN-Is) and an exacerbated release of proinflammatory cytokines, contributes to the severe forms of the disease. SARS-CoV-2 is genetically related to SARS-CoV and Middle East respiratory syndrome-related coronavirus (MERS-CoV), which caused outbreaks in 2003 and 2013, respectively. Although IFN treatment gave some encouraging results against SARS-CoV and MERS-CoV in animal models, its potential as a therapeutic against COVID-19 awaits validation. Here, we describe our current knowledge of the complex interplay between SARS-CoV-2 infection and the IFN system, highlighting some of the gaps that need to be filled for a better understanding of the underlying molecular mechanisms. In addition to the conserved IFN evasion strategies that are likely shared with SARS-CoV and MERS-CoV, novel counteraction mechanisms are being discovered in SARS-CoV-2-infected cells. Since the last coronavirus epidemic, we have made considerable progress in understanding the IFN-I response, including its spatiotemporal regulation and the prominent role of plasmacytoid dendritic cells (pDCs), which are the main IFN-I-producing cells. While awaiting the results of the many clinical trials that are evaluating the efficacy of IFN-I alone or in combination with antiviral molecules, we discuss the potential benefits of a well-timed IFN-I treatment and propose strategies to boost pDC-mediated IFN responses during the early stages of viral infection.
    Keywords covid19
    Publisher WHO
    Document type Article
    Note WHO #Covidence: #691046
    Database COVID19

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  10. Article ; Online: Interplay between SARS-CoV-2 and the type I interferon response

    Sa Ribero, Margarida / Jouvenet, Nolwenn / Dreux, Marlène / Nisole, Sébastien

    ISSN: 1553-7366 ; EISSN: 1553-7374 ; PLoS Pathogens ; https://www.hal.inserm.fr/inserm-02965704 ; PLoS Pathogens, Public Library of Science, 2020, 16 (7), pp.e1008737. ⟨10.1371/journal.ppat.1008737⟩

    2020  

    Abstract: International audience ... The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is responsible for the current COVID-19 pandemic. An unbalanced immune response, characterized by a weak production of type I interferons (IFN-Is) and an ... ...

    Abstract International audience

    The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is responsible for the current COVID-19 pandemic. An unbalanced immune response, characterized by a weak production of type I interferons (IFN-Is) and an exacerbated release of proinflammatory cytokines, contributes to the severe forms of the disease. SARS-CoV-2 is genetically related to SARS-CoV and Middle East respiratory syndrome-related coronavirus (MERS-CoV), which caused outbreaks in 2003 and 2013, respectively. Although IFN treatment gave some encouraging results against SARS-CoV and MERS-CoV in animal models, its potential as a therapeutic against COVID-19 awaits validation. Here, we describe our current knowledge of the complex interplay between SARS-CoV-2 infection and the IFN system, highlighting some of the gaps that need to be filled for a better understanding of the underlying molecular mechanisms. In addition to the conserved IFN evasion strategies that are likely shared with SARS-CoV and MERS-CoV, novel counteraction mechanisms are being discovered in SARS-CoV-2-infected cells. Since the last coronavirus epidemic, we have made considerable progress in understanding the IFN-I response, including its spatiotemporal regulation and the prominent role of plasmacytoid dendritic cells (pDCs), which are the main IFN-I-producing cells. While awaiting the results of the many clinical trials that are evaluating the efficacy of IFN-I alone or in combination with antiviral molecules, we discuss the potential benefits of a well-timed IFN-I treatment and propose strategies to boost pDC-mediated IFN responses during the early stages of viral infection.
    Keywords [SDV.IMM]Life Sciences [q-bio]/Immunology ; [SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology ; [SDV.MHEP.ME]Life Sciences [q-bio]/Human health and pathology/Emerging diseases ; covid19
    Subject code 610
    Language English
    Publishing date 2020-07-29
    Publisher HAL CCSD
    Publishing country fr
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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