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  1. Article ; Online: En garde! The duel functions of MORC3.

    Fox, Lindsey E / Lenschow, Deborah J

    Cell host & microbe

    2022  Volume 30, Issue 1, Page(s) 8–9

    Abstract: Effector-triggered immunity involves "guarded" host processes that, when perturbed by pathogen factors, prompt a secondary response. A recent study published in Nature by Gaidt et al. demonstrates that MORC3 serves as both the guard and the guarded ... ...

    Abstract Effector-triggered immunity involves "guarded" host processes that, when perturbed by pathogen factors, prompt a secondary response. A recent study published in Nature by Gaidt et al. demonstrates that MORC3 serves as both the guard and the guarded antiviral host factor-creating a "heads, I win; tails, you lose!" scenario.
    MeSH term(s) Adenosine Triphosphatases/genetics ; Adenosine Triphosphatases/metabolism ; Antiviral Agents ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Host Microbial Interactions/immunology ; Humans ; Ubiquitin-Protein Ligases ; Virulence Factors/immunology
    Chemical Substances Antiviral Agents ; DNA-Binding Proteins ; Virulence Factors ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Adenosine Triphosphatases (EC 3.6.1.-) ; MORC3 protein, human (EC 3.6.1.-)
    Language English
    Publishing date 2022-01-13
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2278004-X
    ISSN 1934-6069 ; 1931-3128
    ISSN (online) 1934-6069
    ISSN 1931-3128
    DOI 10.1016/j.chom.2021.12.017
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6578: Show issues Location:
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  2. Article ; Online: Context Is Key: Delineating the Unique Functions of IFNα and IFNβ in Disease.

    Fox, Lindsey E / Locke, Marissa C / Lenschow, Deborah J

    Frontiers in immunology

    2020  Volume 11, Page(s) 606874

    Abstract: Type I interferons (IFNs) are critical effector cytokines of the immune system and were originally known for their important role in protecting against viral infections; however, they have more recently been shown to play protective or detrimental roles ... ...

    Abstract Type I interferons (IFNs) are critical effector cytokines of the immune system and were originally known for their important role in protecting against viral infections; however, they have more recently been shown to play protective or detrimental roles in many disease states. Type I IFNs consist of IFNα, IFNβ, IFNϵ, IFNκ, IFNω, and a few others, and they all signal through a shared receptor to exert a wide range of biological activities, including antiviral, antiproliferative, proapoptotic, and immunomodulatory effects. Though the individual type I IFN subtypes possess overlapping functions, there is growing appreciation that they also have unique properties. In this review, we summarize some of the mechanisms underlying differential expression of and signaling by type I IFNs, and we discuss examples of differential functions of IFNα and IFNβ in models of infectious disease, cancer, and autoimmunity.
    MeSH term(s) Animals ; Autoimmune Diseases/immunology ; Autoimmune Diseases/metabolism ; Autoimmunity ; Communicable Diseases/immunology ; Communicable Diseases/metabolism ; Host-Pathogen Interactions ; Humans ; Interferon-alpha/metabolism ; Interferon-beta/metabolism ; Ligands ; Neoplasms/immunology ; Neoplasms/metabolism ; Receptors, Interferon/metabolism ; Signal Transduction ; Tumor Microenvironment
    Chemical Substances Interferon-alpha ; Ligands ; Receptors, Interferon ; Interferon-beta (77238-31-4)
    Language English
    Publishing date 2020-12-21
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2020.606874
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Interferon Alpha, but Not Interferon Beta, Acts Early To Control Chronic Chikungunya Virus Pathogenesis.

    Locke, Marissa C / Fox, Lindsey E / Dunlap, Bria F / Young, Alissa R / Monte, Kristen / Lenschow, Deborah J

    Journal of virology

    2021  Volume 96, Issue 1, Page(s) e0114321

    Abstract: Chikungunya virus (CHIKV) is an arthritogenic alphavirus that causes both debilitating acute and chronic disease. Previous work has shown that type I interferons (IFNs) play a critical role in limiting CHIKV pathogenesis and that interferon alpha (IFN-α) ...

    Abstract Chikungunya virus (CHIKV) is an arthritogenic alphavirus that causes both debilitating acute and chronic disease. Previous work has shown that type I interferons (IFNs) play a critical role in limiting CHIKV pathogenesis and that interferon alpha (IFN-α) and interferon beta (IFN-β) control acute CHIKV infection by distinct mechanisms. However, the role of type I IFNs, especially specific subtypes, during chronic CHIKV disease is unclear. To address this gap in knowledge, we evaluated chronic CHIKV pathogenesis in mice lacking IFN-α or IFN-β. We found that IFN-α was the dominant subtype that controls chronic disease. Despite detecting a varying type I IFN response throughout the course of disease, IFN-α acts within the first few days of infection to control the levels of persistent CHIKV RNA. In addition, using a novel CHIKV-3'-Cre tdTomato reporter system that fate maps CHIKV-infected cells, we showed that IFN-α limits the number of cells that survive CHIKV at sites of dissemination, particularly dermal fibroblasts and immune cells. Though myofibers play a significant role in CHIKV disease, they were not impacted by the loss of IFN-α. Our studies highlight that IFN-α and IFN-β play divergent roles during chronic CHIKV disease through events that occur early in infection and that not all cell types are equally dependent on type I IFNs for restricting viral persistence.
    MeSH term(s) Animals ; Cell Survival ; Chikungunya Fever/metabolism ; Chikungunya Fever/virology ; Chikungunya virus/physiology ; Disease Models, Animal ; Disease Susceptibility ; Host-Pathogen Interactions ; Interferon-alpha/metabolism ; Interferon-beta/metabolism ; Mice ; Mice, Knockout ; RNA, Viral ; Virus Replication
    Chemical Substances Interferon-alpha ; RNA, Viral ; Interferon-beta (77238-31-4)
    Language English
    Publishing date 2021-10-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80174-4
    ISSN 1098-5514 ; 0022-538X
    ISSN (online) 1098-5514
    ISSN 0022-538X
    DOI 10.1128/JVI.01143-21
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 609: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Fibroblast growth factor-9 expression in airway epithelial cells amplifies the type I interferon response and alters influenza A virus pathogenesis.

    Hiller, Bradley E / Yin, Yongjun / Perng, Yi-Chieh / de Araujo Castro, Ítalo / Fox, Lindsey E / Locke, Marissa C / Monte, Kristen J / López, Carolina B / Ornitz, David M / Lenschow, Deborah J

    PLoS pathogens

    2022  Volume 18, Issue 6, Page(s) e1010228

    Abstract: Influenza A virus (IAV) preferentially infects conducting airway and alveolar epithelial cells in the lung. The outcome of these infections is impacted by the host response, including the production of various cytokines, chemokines, and growth factors. ... ...

    Abstract Influenza A virus (IAV) preferentially infects conducting airway and alveolar epithelial cells in the lung. The outcome of these infections is impacted by the host response, including the production of various cytokines, chemokines, and growth factors. Fibroblast growth factor-9 (FGF9) is required for lung development, can display antiviral activity in vitro, and is upregulated in asymptomatic patients during early IAV infection. We therefore hypothesized that FGF9 would protect the lungs from respiratory virus infection and evaluated IAV pathogenesis in mice that overexpress FGF9 in club cells in the conducting airway epithelium (FGF9-OE mice). However, we found that FGF9-OE mice were highly susceptible to IAV and Sendai virus infection compared to control mice. FGF9-OE mice displayed elevated and persistent viral loads, increased expression of cytokines and chemokines, and increased numbers of infiltrating immune cells as early as 1 day post-infection (dpi). Gene expression analysis showed an elevated type I interferon (IFN) signature in the conducting airway epithelium and analysis of IAV tropism uncovered a dramatic shift in infection from the conducting airway epithelium to the alveolar epithelium in FGF9-OE lungs. These results demonstrate that FGF9 signaling primes the conducting airway epithelium to rapidly induce a localized IFN and proinflammatory cytokine response during viral infection. Although this response protects the airway epithelial cells from IAV infection, it allows for early and enhanced infection of the alveolar epithelium, ultimately leading to increased morbidity and mortality. Our study illuminates a novel role for FGF9 in regulating respiratory virus infection and pathogenesis.
    MeSH term(s) Animals ; Cytokines/metabolism ; Epithelial Cells/metabolism ; Fibroblast Growth Factor 9/biosynthesis ; Humans ; Influenza A virus/metabolism ; Influenza, Human/metabolism ; Influenza, Human/virology ; Interferon Type I/metabolism ; Mice ; Orthomyxoviridae Infections/metabolism ; Orthomyxoviridae Infections/virology
    Chemical Substances Cytokines ; FGF9 protein, human ; Fgf9 protein, mouse ; Fibroblast Growth Factor 9 ; Interferon Type I
    Language English
    Publishing date 2022-06-08
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2205412-1
    ISSN 1553-7374 ; 1553-7374
    ISSN (online) 1553-7374
    ISSN 1553-7374
    DOI 10.1371/journal.ppat.1010228
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Commensal Cryptosporidium colonization elicits a cDC1-dependent Th1 response that promotes intestinal homeostasis and limits other infections.

    Russler-Germain, Emilie V / Jung, Jisun / Miller, Aidan T / Young, Shannon / Yi, Jaeu / Wehmeier, Alec / Fox, Lindsey E / Monte, Kristen J / Chai, Jiani N / Kulkarni, Devesha H / Funkhouser-Jones, Lisa J / Wilke, Georgia / Durai, Vivek / Zinselmeyer, Bernd H / Czepielewski, Rafael S / Greco, Suellen / Murphy, Kenneth M / Newberry, Rodney D / Sibley, L David /
    Hsieh, Chyi-Song

    Immunity

    2021  Volume 54, Issue 11, Page(s) 2547–2564.e7

    Abstract: Cryptosporidium can cause severe diarrhea and morbidity, but many infections are asymptomatic. Here, we studied the immune response to a commensal strain of Cryptosporidium tyzzeri (Ct-STL) serendipitously discovered when conventional type 1 dendritic ... ...

    Abstract Cryptosporidium can cause severe diarrhea and morbidity, but many infections are asymptomatic. Here, we studied the immune response to a commensal strain of Cryptosporidium tyzzeri (Ct-STL) serendipitously discovered when conventional type 1 dendritic cell (cDC1)-deficient mice developed cryptosporidiosis. Ct-STL was vertically transmitted without negative health effects in wild-type mice. Yet, Ct-STL provoked profound changes in the intestinal immune system, including induction of an IFN-γ-producing Th1 response. TCR sequencing coupled with in vitro and in vivo analysis of common Th1 TCRs revealed that Ct-STL elicited a dominant antigen-specific Th1 response. In contrast, deficiency in cDC1s skewed the Ct-STL CD4 T cell response toward Th17 and regulatory T cells. Although Ct-STL predominantly colonized the small intestine, colon Th1 responses were enhanced and associated with protection against Citrobacter rodentium infection and exacerbation of dextran sodium sulfate and anti-IL10R-triggered colitis. Thus, Ct-STL represents a commensal pathobiont that elicits Th1-mediated intestinal homeostasis that may reflect asymptomatic human Cryptosporidium infection.
    MeSH term(s) Animals ; Cryptosporidiosis/immunology ; Cryptosporidiosis/parasitology ; Cryptosporidium/immunology ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Disease Models, Animal ; Homeostasis ; Host-Parasite Interactions/immunology ; Intestinal Mucosa/immunology ; Intestinal Mucosa/metabolism ; Intestinal Mucosa/parasitology ; Mice ; Microbiota ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism ; Th1 Cells/immunology ; Th1 Cells/metabolism
    Language English
    Publishing date 2021-10-28
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2021.10.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4227: Show issues Location:
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