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  1. Article ; Online: The gene regulatory basis of bystander activation in CD8

    Watson, Neva B / Patel, Ravi K / Kean, Connor / Veazey, Janelle / Oyesola, Oyebola O / Laniewski, Nathan / Grenier, Jennifer K / Wang, Jocelyn / Tabilas, Cybelle / Yee Mon, Kristel J / McNairn, Adrian J / Peng, Seth A / Wesnak, Samantha P / Nzingha, Kito / Davenport, Miles P / Tait Wojno, Elia D / Scheible, Kristin M / Smith, Norah L / Grimson, Andrew /
    Rudd, Brian D

    Science immunology

    2024  Volume 9, Issue 92, Page(s) eadf8776

    Abstract: ... ...

    Abstract CD8
    MeSH term(s) Humans ; Adult ; Mice ; Animals ; CD8-Positive T-Lymphocytes ; Immunity, Innate ; Cytokines ; T-Lymphocyte Subsets ; Antigens
    Chemical Substances Cytokines ; Antigens
    Language English
    Publishing date 2024-02-23
    Publishing country United States
    Document type Journal Article
    ISSN 2470-9468
    ISSN (online) 2470-9468
    DOI 10.1126/sciimmunol.adf8776
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The influence of macrophage growth factors on Theiler's Murine Encephalomyelitis Virus (TMEV) infection and activation of macrophages.

    Schneider, Karin M / Watson, Neva B / Minchenberg, Scott B / Massa, Paul T

    Cytokine

    2017  Volume 102, Page(s) 83–93

    Abstract: Macrophages are common targets for infection and innate immune activation by many pathogenic viruses including the neurotropic Theiler's Murine Encephalomyelitis Virus (TMEV). As both infection and innate activation of macrophages are key determinants of ...

    Abstract Macrophages are common targets for infection and innate immune activation by many pathogenic viruses including the neurotropic Theiler's Murine Encephalomyelitis Virus (TMEV). As both infection and innate activation of macrophages are key determinants of viral pathogenesis especially in the central nervous system (CNS), an analysis of macrophage growth factors on these events was performed. C3H mouse bone-marrow cells were differentiated in culture using either recombinant macrophage colony stimulating factor (M-CSF) or granulocyte-macrophage colony-stimulating factor (GM-CSF), inoculated with TMEV (BeAn) and analyzed at various times thereafter. Cytokine RNA and protein analysis, virus titers, and flow cytometry were performed to characterize virological parameters under these culture conditions. GM-CSF-differentiated macrophages showed higher levels of TMEV viral RNA and proinflammatory molecules compared to infected M-CSF-differentiated cells. Thus, GM-CSF increases both TMEV infection and TMEV-induced activation of macrophages compared to that seen with M-CSF. Moreover, while infectious viral particles decreased from a peak at 12h to undetectable levels at 48h post infection, TMEV viral RNA remained higher in GM-CSF- compared to M-CSF-differentiated macrophages in concert with increased proinflammatory gene expression. Analysis of a possible basis for these differences determined that glycolytic rates contributed to heightened virus replication and proinflammatory cytokine secretion in GM-CSF compared to M-CSF-differentiated macrophages. In conclusion, we provide evidence implicating a role for GM-CSF in promoting virus replication and proinflammatory cytokine expression in macrophages, indicating that GM-CSF may be a key factor for TMEV infection and the induction of chronic TMEV-induced immunopathogenesis in the CNS.
    MeSH term(s) Animals ; Cardiovirus Infections/etiology ; Cardiovirus Infections/immunology ; Cardiovirus Infections/virology ; Cell Differentiation/immunology ; Chemokines/genetics ; Chemokines/metabolism ; Cytokines/genetics ; Cytokines/metabolism ; Glycolysis ; Granulocyte-Macrophage Colony-Stimulating Factor/immunology ; Macrophage Activation ; Macrophage Colony-Stimulating Factor/immunology ; Macrophages/immunology ; Macrophages/pathology ; Macrophages/virology ; Mice ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; RNA, Viral/genetics ; Theilovirus/genetics ; Theilovirus/isolation & purification ; Theilovirus/pathogenicity ; Virus Replication/immunology
    Chemical Substances Chemokines ; Cytokines ; RNA, Messenger ; RNA, Viral ; Macrophage Colony-Stimulating Factor (81627-83-0) ; Granulocyte-Macrophage Colony-Stimulating Factor (83869-56-1)
    Language English
    Publishing date 2017-08-09
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1018055-2
    ISSN 1096-0023 ; 1043-4666
    ISSN (online) 1096-0023
    ISSN 1043-4666
    DOI 10.1016/j.cyto.2017.07.015
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    Zs.A 2840: Show issues Location:
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  3. Article ; Online: SHP-1-dependent macrophage differentiation exacerbates virus-induced myositis.

    Watson, Neva B / Schneider, Karin M / Massa, Paul T

    Journal of immunology (Baltimore, Md. : 1950)

    2015  Volume 194, Issue 6, Page(s) 2796–2809

    Abstract: Virus-induced myositis is an emerging global affliction that remains poorly characterized with few treatment options. Moreover, muscle-tropic viruses often spread to the CNS, causing dramatically increased morbidity. Therefore, there is an urgent need to ...

    Abstract Virus-induced myositis is an emerging global affliction that remains poorly characterized with few treatment options. Moreover, muscle-tropic viruses often spread to the CNS, causing dramatically increased morbidity. Therefore, there is an urgent need to explore genetic factors involved in this class of human disease. This report investigates critical innate immune pathways affecting murine virus-induced myositis. Of particular importance, the key immune regulator src homology region 2 domain-containing phosphatase 1 (SHP-1), which normally suppresses macrophage-mediated inflammation, is a major factor in promoting clinical disease in muscle. We show that Theiler's murine encephalomyelitis virus (TMEV) infection of skeletal myofibers induces inflammation and subsequent dystrophic calcification, with loss of ambulation in wild-type (WT) mice. Surprisingly, although similar extensive myofiber infection and inflammation are observed in SHP-1(-/-) mice, these mice neither accumulate dead calcified myofibers nor lose ambulation. Macrophages were the predominant effector cells infiltrating WT and SHP-1(-/-) muscle, and an increased infiltration of immature monocytes/macrophages correlated with an absence of clinical disease in SHP-1(-/-) mice, whereas mature M1-like macrophages corresponded with increased myofiber degeneration in WT mice. Furthermore, blocking SHP-1 activation in WT macrophages blocked virus-induced myofiber degeneration, and pharmacologic ablation of macrophages inhibited muscle calcification in TMEV-infected WT animals. These data suggest that, following TMEV infection of muscle, SHP-1 promotes M1 differentiation of infiltrating macrophages, and these inflammatory macrophages are likely involved in damaging muscle fibers. These findings reveal a pathological role for SHP-1 in promoting inflammatory macrophage differentiation and myofiber damage in virus-infected skeletal muscle, thus identifying SHP-1 and M1 macrophages as essential mediators of virus-induced myopathy.
    MeSH term(s) Animals ; Antibodies, Neutralizing/immunology ; Antibodies, Neutralizing/pharmacology ; CD47 Antigen/immunology ; CD47 Antigen/metabolism ; Cardiovirus Infections/genetics ; Cardiovirus Infections/immunology ; Cardiovirus Infections/virology ; Cell Differentiation/genetics ; Cell Differentiation/immunology ; Flow Cytometry ; Host-Pathogen Interactions/drug effects ; Host-Pathogen Interactions/immunology ; Humans ; Macrophages/immunology ; Macrophages/metabolism ; Macrophages/pathology ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Knockout ; Microscopy, Fluorescence ; Monocytes/immunology ; Monocytes/metabolism ; Monocytes/pathology ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Muscle, Skeletal/virology ; Myositis/genetics ; Myositis/immunology ; Myositis/virology ; Oligonucleotide Array Sequence Analysis ; Protein Tyrosine Phosphatase, Non-Receptor Type 6/deficiency ; Protein Tyrosine Phosphatase, Non-Receptor Type 6/genetics ; Protein Tyrosine Phosphatase, Non-Receptor Type 6/immunology ; Theilovirus/immunology ; Theilovirus/physiology ; Transcriptome/immunology ; Virus Replication/immunology
    Chemical Substances Antibodies, Neutralizing ; CD47 Antigen ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 (EC 3.1.3.48) ; Ptpn6 protein, mouse (EC 3.1.3.48)
    Language English
    Publishing date 2015-03-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.1402210
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    Ud II Zs.37: Show issues Location:
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    Zs.MG 28: Show issues

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  4. Article ; Online: Differential Sensitivity to IL-12 Drives Sex-Specific Differences in the CD8+ T Cell Response to Infection.

    Yee Mon, Kristel Joy / Goldsmith, Elizabeth / Watson, Neva B / Wang, Jocelyn / Smith, Norah L / Rudd, Brian D

    ImmunoHorizons

    2019  Volume 3, Issue 4, Page(s) 121–132

    Abstract: It is well known that males and females respond differently to intracellular pathogens. Females mount a more robust immune response than males, which decreases their susceptibility to infection but comes at the cost of increasing immunopathology. However, ...

    Abstract It is well known that males and females respond differently to intracellular pathogens. Females mount a more robust immune response than males, which decreases their susceptibility to infection but comes at the cost of increasing immunopathology. However, the underlying basis for sex-specific differences in the CD8
    MeSH term(s) Adoptive Transfer ; Animals ; Antigens/immunology ; CD8-Positive T-Lymphocytes/cytology ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/metabolism ; Cell Differentiation/immunology ; Disease Models, Animal ; Female ; Host-Pathogen Interactions/immunology ; Immunophenotyping ; Infections/etiology ; Infections/metabolism ; Interleukin-12/metabolism ; Male ; Mice ; Mice, Knockout ; Sex Factors
    Chemical Substances Antigens ; Interleukin-12 (187348-17-0)
    Language English
    Publishing date 2019-07-17
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ISSN 2573-7732
    ISSN (online) 2573-7732
    DOI 10.4049/immunohorizons.1800066
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  5. Article ; Online: Fetal and adult progenitors give rise to unique populations of CD8+ T cells.

    Wang, Jocelyn / Wissink, Erin M / Watson, Neva B / Smith, Norah L / Grimson, Andrew / Rudd, Brian D

    Blood

    2016  Volume 128, Issue 26, Page(s) 3073–3082

    Abstract: During the ontogeny of the mammalian immune system, distinct lineages of cells arise from fetal and adult hematopoietic stem cells (HSCs) during specific stages of development. However, in some cases, the same immune cell type is produced by both HSC ... ...

    Abstract During the ontogeny of the mammalian immune system, distinct lineages of cells arise from fetal and adult hematopoietic stem cells (HSCs) during specific stages of development. However, in some cases, the same immune cell type is produced by both HSC populations, resulting in the generation of phenotypically similar cells with distinct origins and divergent functional properties. In this report, we demonstrate that neonatal CD8
    MeSH term(s) Adult Stem Cells/cytology ; Adult Stem Cells/metabolism ; Aging ; Animals ; Animals, Newborn ; Biomarkers/metabolism ; CD8-Positive T-Lymphocytes/cytology ; DNA-Binding Proteins/metabolism ; Fetal Stem Cells/cytology ; Fetal Stem Cells/metabolism ; Fetus/cytology ; Gene Expression Profiling ; Immunologic Memory ; Mice, Inbred C57BL ; Phenotype ; RNA-Binding Proteins ; Thymus Gland/cytology
    Chemical Substances Biomarkers ; DNA-Binding Proteins ; Lin28b protein, mouse ; RNA-Binding Proteins
    Language English
    Publishing date 2016-11-15
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2016-06-725366
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    Uh III Zs.140: Show issues Location:
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  6. Article ; Online: Developmental Origin Governs CD8

    Smith, Norah L / Patel, Ravi K / Reynaldi, Arnold / Grenier, Jennifer K / Wang, Jocelyn / Watson, Neva B / Nzingha, Kito / Yee Mon, Kristel J / Peng, Seth A / Grimson, Andrew / Davenport, Miles P / Rudd, Brian D

    Cell

    2018  Volume 174, Issue 1, Page(s) 117–130.e14

    Abstract: Heterogeneity is a hallmark feature of the adaptive immune system in vertebrates. Following infection, naive T cells differentiate into various subsets of effector and memory T cells, which help to eliminate pathogens and maintain long-term immunity. The ...

    Abstract Heterogeneity is a hallmark feature of the adaptive immune system in vertebrates. Following infection, naive T cells differentiate into various subsets of effector and memory T cells, which help to eliminate pathogens and maintain long-term immunity. The current model suggests there is a single lineage of naive T cells that give rise to different populations of effector and memory T cells depending on the type and amounts of stimulation they encounter during infection. Here, we have discovered that multiple sub-populations of cells exist in the naive CD8
    MeSH term(s) Animals ; CD8-Positive T-Lymphocytes/drug effects ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/metabolism ; Cell Differentiation ; Cell Line, Tumor ; Chromatin/metabolism ; Cytokines/pharmacology ; Epitopes, T-Lymphocyte/genetics ; Epitopes, T-Lymphocyte/metabolism ; Genes, Developmental ; Immunologic Memory ; Interferon-gamma/metabolism ; Killer Cells, Natural/cytology ; Killer Cells, Natural/metabolism ; Listeria monocytogenes/metabolism ; Listeria monocytogenes/pathogenicity ; Mice ; Mice, Inbred C57BL ; Principal Component Analysis ; T-Lymphocyte Subsets/cytology ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism ; Thymus Gland/transplantation ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transcriptome
    Chemical Substances Chromatin ; Cytokines ; Epitopes, T-Lymphocyte ; Transcription Factors ; Interferon-gamma (82115-62-6)
    Language English
    Publishing date 2018-06-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2018.05.029
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    Zs.A 1167: Show issues Location:
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    Zs.MG 58: Show issues

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