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  1. Article ; Online: NKG2C/E Marks the Unique Cytotoxic CD4 T Cell Subset, ThCTL, Generated by Influenza Infection.

    Marshall, Nikki B / Vong, Allen M / Devarajan, Priyadharshini / Brauner, Matthew D / Kuang, Yi / Nayar, Ribhu / Schutten, Elizabeth A / Castonguay, Catherine H / Berg, Leslie J / Nutt, Stephen L / Swain, Susan L

    Journal of immunology (Baltimore, Md. : 1950)

    2016  Volume 198, Issue 3, Page(s) 1142–1155

    Abstract: CD4 T cells can differentiate into multiple effector subsets, including ThCTL that mediate MHC class II-restricted cytotoxicity. Although CD4 T cell-mediated cytotoxicity has been reported in multiple viral infections, their characteristics and the ... ...

    Abstract CD4 T cells can differentiate into multiple effector subsets, including ThCTL that mediate MHC class II-restricted cytotoxicity. Although CD4 T cell-mediated cytotoxicity has been reported in multiple viral infections, their characteristics and the factors regulating their generation are unclear, in part due to a lack of a signature marker. We show in this article that, in mice, NKG2C/E identifies the ThCTL that develop in the lung during influenza A virus infection. ThCTL express the NKG2X/CD94 complex, in particular the NKG2C/E isoforms. NKG2C/E
    MeSH term(s) Animals ; Biomarkers/analysis ; CD4-Positive T-Lymphocytes/chemistry ; CD4-Positive T-Lymphocytes/classification ; CD4-Positive T-Lymphocytes/immunology ; Cytotoxicity, Immunologic ; Influenza A virus ; Interferon-gamma/biosynthesis ; Lung/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; NK Cell Lectin-Like Receptor Subfamily C/analysis ; Orthomyxoviridae Infections/immunology ; Positive Regulatory Domain I-Binding Factor 1 ; Transcription Factors/analysis
    Chemical Substances Biomarkers ; Klrc2 protein, mouse ; NK Cell Lectin-Like Receptor Subfamily C ; Prdm1 protein, mouse ; Transcription Factors ; Interferon-gamma (82115-62-6) ; Positive Regulatory Domain I-Binding Factor 1 (EC 2.1.1.-)
    Language English
    Publishing date 2016-12-28
    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.1601297
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ud II Zs.37: Show issues Location:
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  2. Article ; Online: IRF4 Regulates the Ratio of T-Bet to Eomesodermin in CD8+ T Cells Responding to Persistent LCMV Infection.

    Nayar, Ribhu / Schutten, Elizabeth / Jangalwe, Sonal / Durost, Philip A / Kenney, Laurie L / Conley, James M / Daniels, Keith / Brehm, Michael A / Welsh, Raymond M / Berg, Leslie J

    PloS one

    2015  Volume 10, Issue 12, Page(s) e0144826

    Abstract: CD8+ T cell exhaustion commonly occurs in chronic infections and cancers. During T cell exhaustion there is a progressive and hierarchical loss of effector cytokine production, up-regulation of inhibitory co-stimulatory molecules, and eventual deletion ... ...

    Abstract CD8+ T cell exhaustion commonly occurs in chronic infections and cancers. During T cell exhaustion there is a progressive and hierarchical loss of effector cytokine production, up-regulation of inhibitory co-stimulatory molecules, and eventual deletion of antigen specific cells by apoptosis. A key factor that regulates T cell exhaustion is persistent TCR stimulation. Loss of this interaction results in restoration of CD8+ T cell effector functions in previously exhausted CD8+ T cells. TCR stimulation is also important for the differentiation of Eomeshi anti-viral CD8+ effector T cells from T-bethi precursors, both of which are required for optimal viral control. However, the molecular mechanisms regulating the differentiation of these two cell subsets and the relative ratios required for viral clearance have not been described. We show that TCR signal strength regulates the relative expression of T-bet and Eomes in antigen-specific CD8+ T cells by modulating levels of IRF4. Reduced IRF4 expression results in skewing of this ratio in the favor of Eomes, leading to lower proportions and numbers of T-bet+ Eomes- precursors and poor control of LCMV-clone 13 infection. Manipulation of this ratio in the favor of T-bet restores the differentiation of T-bet+ Eomes- precursors and the protective balance of T-bet to Eomes required for efficient viral control. These data highlight a critical role for IRF4 in regulating protective anti-viral CD8+ T cell responses by ensuring a balanced ratio of T-bet to Eomes, leading to the ultimate control of this chronic viral infection.
    MeSH term(s) Amino Acid Sequence ; Animals ; CD8-Positive T-Lymphocytes/cytology ; CD8-Positive T-Lymphocytes/metabolism ; Cell Differentiation ; Cell Line ; Cricetinae ; Gene Expression Regulation ; Interferon Regulatory Factors/metabolism ; Lymphocytic choriomeningitis virus/physiology ; Male ; Mice ; Molecular Sequence Data ; Signal Transduction ; T-Box Domain Proteins/metabolism
    Chemical Substances Eomes protein, mouse ; Interferon Regulatory Factors ; T-Box Domain Proteins ; T-box transcription factor TBX21 ; interferon regulatory factor-4
    Language English
    Publishing date 2015-12-29
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0144826
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Relapsing-remitting central nervous system autoimmunity mediated by GFAP-specific CD8 T cells.

    Sasaki, Katsuhiro / Bean, Angela / Shah, Shivanee / Schutten, Elizabeth / Huseby, Priya G / Peters, Bjorn / Shen, Zu T / Vanguri, Vijay / Liggitt, Denny / Huseby, Eric S

    Journal of immunology (Baltimore, Md. : 1950)

    2014  Volume 192, Issue 7, Page(s) 3029–3042

    Abstract: Multiple sclerosis (MS) is an inflammatory disease of the CNS that causes the demyelination of nerve cells and destroys oligodendrocytes, neurons, and axons. Historically, MS has been thought to be a CD4 T cell-mediated autoimmune disease of CNS white ... ...

    Abstract Multiple sclerosis (MS) is an inflammatory disease of the CNS that causes the demyelination of nerve cells and destroys oligodendrocytes, neurons, and axons. Historically, MS has been thought to be a CD4 T cell-mediated autoimmune disease of CNS white matter. However, recent studies identified CD8 T cell infiltrates and gray matter lesions in MS patients. These findings suggest that CD8 T cells and CNS Ags other than myelin proteins may be involved during the MS disease process. In this article, we show that CD8 T cells reactive to glial fibrillary acidic protein (GFAP), a protein expressed in astrocytes, can avoid tolerance mechanisms and, depending upon the T cell-triggering event, drive unique aspects of inflammatory CNS autoimmunity. In GFAP-specific CD8 TCR-transgenic (BG1) mice, tissue resident memory-like CD8 T cells spontaneously infiltrate the gray matter and white matter of the CNS, resulting in a relapsing-remitting CNS autoimmunity. The frequency, severity, and remissions from spontaneous disease are controlled by the presence of polyclonal B cells. In contrast, a viral trigger induces GFAP-specific CD8 T effector cells to exclusively target the meninges and vascular/perivascular space of the gray and white matter of the brain, causing a rapid, acute CNS disease. These findings demonstrate that the type of CD8 T cell-triggering event can determine the presentation of distinct CNS autoimmune disease pathologies.
    MeSH term(s) Animals ; Astrocytes/immunology ; Astrocytes/metabolism ; Astrocytes/pathology ; Autoimmunity/immunology ; Brain/immunology ; Brain/metabolism ; Brain/pathology ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/metabolism ; CD8-Positive T-Lymphocytes/pathology ; Cells, Cultured ; Central Nervous System/immunology ; Central Nervous System/metabolism ; Central Nervous System/pathology ; Central Nervous System Diseases/genetics ; Central Nervous System Diseases/immunology ; Central Nervous System Diseases/metabolism ; Flow Cytometry ; Glial Fibrillary Acidic Protein/genetics ; Glial Fibrillary Acidic Protein/immunology ; Glial Fibrillary Acidic Protein/metabolism ; Immunohistochemistry ; Interferon-gamma/immunology ; Interferon-gamma/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Mice, Knockout ; Mice, Transgenic ; Multiple Sclerosis/genetics ; Multiple Sclerosis/immunology ; Multiple Sclerosis/metabolism ; Receptors, Antigen, T-Cell/genetics ; Receptors, Antigen, T-Cell/immunology ; Receptors, Antigen, T-Cell/metabolism ; Spinal Cord/immunology ; Spinal Cord/metabolism ; Spinal Cord/pathology
    Chemical Substances Glial Fibrillary Acidic Protein ; Receptors, Antigen, T-Cell ; Interferon-gamma (82115-62-6)
    Language English
    Publishing date 2014-03-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    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.1302911
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  4. Article ; Online: Graded levels of IRF4 regulate CD8+ T cell differentiation and expansion, but not attrition, in response to acute virus infection.

    Nayar, Ribhu / Schutten, Elizabeth / Bautista, Bianca / Daniels, Keith / Prince, Amanda L / Enos, Megan / Brehm, Michael A / Swain, Susan L / Welsh, Raymond M / Berg, Leslie J

    Journal of immunology (Baltimore, Md. : 1950)

    2014  Volume 192, Issue 12, Page(s) 5881–5893

    Abstract: In response to acute virus infections, CD8(+) T cells differentiate to form a large population of short-lived effectors and a stable pool of long-lived memory cells. The characteristics of the CD8(+) T cell response are influenced by TCR affinity, Ag ... ...

    Abstract In response to acute virus infections, CD8(+) T cells differentiate to form a large population of short-lived effectors and a stable pool of long-lived memory cells. The characteristics of the CD8(+) T cell response are influenced by TCR affinity, Ag dose, and the inflammatory cytokine milieu dictated by the infection. To address the mechanism by which differences in TCR signal strength could regulate CD8(+) T cell differentiation, we investigated the transcription factor, IFN regulatory factor 4 (IRF4). We show that IRF4 is transiently upregulated to differing levels in murine CD8(+) T cells, based on the strength of TCR signaling. In turn, IRF4 controls the magnitude of the CD8(+) T cell response to acute virus infection in a dose-dependent manner. Modest differences in IRF4 expression dramatically influence the numbers of short-lived effector cells at the peak of the infection, but have no impact on the kinetics of the infection or on the rate of T cell contraction. Furthermore, the expression of key transcription factors such as T cell factor 1 and Eomesodermin are highly sensitive to graded levels of IRF4. In contrast, T-bet expression is less dependent on IRF4 levels and is influenced by the nature of the infection. These data indicate that IRF4 is a key component that translates the strength of TCR signaling into a graded response of virus-specific CD8(+) T cells.
    MeSH term(s) Acute Disease ; Animals ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/pathology ; Cell Differentiation/genetics ; Cell Differentiation/immunology ; Cell Proliferation ; Influenza A virus/genetics ; Influenza A virus/immunology ; Interferon Regulatory Factors/genetics ; Interferon Regulatory Factors/immunology ; Lymphocytic Choriomeningitis/genetics ; Lymphocytic Choriomeningitis/immunology ; Lymphocytic choriomeningitis virus/genetics ; Lymphocytic choriomeningitis virus/immunology ; Mice ; Mice, Knockout ; Orthomyxoviridae Infections/genetics ; Orthomyxoviridae Infections/immunology ; Receptors, Antigen, T-Cell/genetics ; Receptors, Antigen, T-Cell/immunology ; Signal Transduction/genetics ; Signal Transduction/immunology ; Up-Regulation/genetics ; Up-Regulation/immunology
    Chemical Substances Interferon Regulatory Factors ; Receptors, Antigen, T-Cell ; interferon regulatory factor-4
    Language English
    Publishing date 2014-05-16
    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.1303187
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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