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  1. Article ; Online: I-A

    Stadinski, Brian D / Cleveland, Sarah B / Brehm, Michael A / Greiner, Dale L / Huseby, Priya G / Huseby, Eric S

    Nature immunology

    2023  Volume 24, Issue 4, Page(s) 652–663

    Abstract: Genetic susceptibility to type 1 diabetes is associated with homozygous expression of major histocompatibility complex class II alleles that carry specific beta chain polymorphisms. Why heterozygous expression of these major histocompatibility complex ... ...

    Abstract Genetic susceptibility to type 1 diabetes is associated with homozygous expression of major histocompatibility complex class II alleles that carry specific beta chain polymorphisms. Why heterozygous expression of these major histocompatibility complex class II alleles does not confer a similar predisposition is unresolved. Using a nonobese diabetic mouse model, here we show that heterozygous expression of the type 1 diabetes-protective allele I-A
    MeSH term(s) Mice ; Animals ; Diabetes Mellitus, Type 1 ; CD4-Positive T-Lymphocytes ; CD8-Positive T-Lymphocytes ; Histocompatibility Antigens Class II ; Insulin/metabolism ; Mice, Inbred NOD
    Chemical Substances Histocompatibility Antigens Class II ; Insulin
    Language English
    Publishing date 2023-02-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-023-01441-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5294: Show issues Location:
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  2. Article ; Online: A temporal thymic selection switch and ligand binding kinetics constrain neonatal Foxp3

    Stadinski, Brian D / Blevins, Sydney J / Spidale, Nicholas A / Duke, Brian R / Huseby, Priya G / Stern, Lawrence J / Huseby, Eric S

    Nature immunology

    2019  Volume 20, Issue 8, Page(s) 1046–1058

    Abstract: The neonatal thymus generates ... ...

    Abstract The neonatal thymus generates Foxp3
    MeSH term(s) Animals ; Autoantigens/immunology ; Autoimmunity/immunology ; Cell Differentiation/immunology ; Cell Line ; Female ; Forkhead Transcription Factors/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Protein-Arginine Deiminases/metabolism ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; Self Tolerance/immunology ; T-Lymphocytes, Regulatory/cytology ; T-Lymphocytes, Regulatory/immunology ; Thymus Gland/cytology
    Chemical Substances Autoantigens ; Forkhead Transcription Factors ; Foxp3 protein, mouse ; Receptors, Antigen, T-Cell, alpha-beta ; Padi4 protein, mouse (EC 3.5.3.15) ; Protein-Arginine Deiminases (EC 3.5.3.15)
    Language English
    Publishing date 2019-06-17
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-019-0414-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Pathogenic CD8 T cells in multiple sclerosis and its experimental models.

    Huseby, Eric S / Huseby, Priya G / Shah, Shivanee / Smith, Rebecca / Stadinski, Brian D

    Frontiers in immunology

    2012  Volume 3, Page(s) 64

    Abstract: A growing body of evidence suggests that autoreactive CD8 T cells contribute to the disease process in multiple sclerosis (MS). Lymphocytes in MS plaques are biased toward the CD8 lineage, and MS patients harbor CD8 T cells specific for multiple central ... ...

    Abstract A growing body of evidence suggests that autoreactive CD8 T cells contribute to the disease process in multiple sclerosis (MS). Lymphocytes in MS plaques are biased toward the CD8 lineage, and MS patients harbor CD8 T cells specific for multiple central nervous system (CNS) antigens. Currently, there are relatively few experimental model systems available to study these pathogenic CD8 T cells in vivo. However, the few studies that have been done characterizing the mechanisms used by CD8 T cells to induce CNS autoimmunity indicate that several of the paradigms of how CD4 T cells mediate CNS autoimmunity do not hold true for CD8 T cells or for patients with MS. Thus, myelin-specific CD4 T cells are likely to be one of several important mechanisms that drive CNS disease in MS patients. The focus of this review is to highlight the current models of pathogenic CNS-reactive CD8 T cells and the molecular mechanisms these lymphocytes use when causing CNS inflammation and damage. Understanding how CNS-reactive CD8 T cells escape tolerance induction and induce CNS autoimmunity is critical to our ability to propose and test new therapies for MS.
    Language English
    Publishing date 2012-03-29
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2012.00064
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Effect of CDR3 sequences and distal V gene residues in regulating TCR-MHC contacts and ligand specificity.

    Stadinski, Brian D / Trenh, Peter / Duke, Brian / Huseby, Priya G / Li, Guoqi / Stern, Lawrence J / Huseby, Eric S

    Journal of immunology (Baltimore, Md. : 1950)

    2014  Volume 192, Issue 12, Page(s) 6071–6082

    Abstract: The mature T cell repertoire has the ability to orchestrate immunity to a wide range of potential pathogen challenges. This ability stems from thymic development producing individual T cell clonotypes that express TCRs with unique patterns of Ag ... ...

    Abstract The mature T cell repertoire has the ability to orchestrate immunity to a wide range of potential pathogen challenges. This ability stems from thymic development producing individual T cell clonotypes that express TCRs with unique patterns of Ag reactivity. The Ag specificity of TCRs is created from the combinatorial pairing of one of a set of germline encoded TCR Vα and Vβ gene segments with randomly created CDR3 sequences. How the amalgamation of germline encoded and randomly created TCR sequences results in Ag receptors with unique patterns of ligand specificity is not fully understood. Using cellular, biophysical, and structural analyses, we show that CDR3α residues can modulate the geometry in which TCRs bind peptide-MHC (pMHC), governing whether and how germline encoded TCR Vα and Vβ residues interact with MHC. In addition, a CDR1α residue that is positioned distal to the TCR-pMHC binding interface is shown to contribute to the peptide specificity of T cells. These findings demonstrate that the specificity of individual T cell clonotypes arises not only from TCR residues that create direct contacts with the pMHC, but also from a collection of indirect effects that modulate how TCR residues are used to bind pMHC.
    MeSH term(s) Animals ; Complementarity Determining Regions/chemistry ; Complementarity Determining Regions/genetics ; Complementarity Determining Regions/immunology ; Histocompatibility Antigens/chemistry ; Histocompatibility Antigens/genetics ; Histocompatibility Antigens/immunology ; Mice ; Mice, Knockout ; Peptides/chemistry ; Peptides/genetics ; Peptides/immunology ; Receptors, Antigen, T-Cell, alpha-beta/chemistry ; Receptors, Antigen, T-Cell, alpha-beta/genetics ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; T-Lymphocytes/chemistry ; T-Lymphocytes/immunology
    Chemical Substances Complementarity Determining Regions ; Histocompatibility Antigens ; Peptides ; Receptors, Antigen, T-Cell, alpha-beta
    Language English
    Publishing date 2014-05-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    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.1303209
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  5. Article ; Online: A role for differential variable gene pairing in creating T cell receptors specific for unique major histocompatibility ligands.

    Stadinski, Brian D / Trenh, Peter / Smith, Rebecca L / Bautista, Bianca / Huseby, Priya G / Li, Guoqi / Stern, Lawrence J / Huseby, Eric S

    Immunity

    2011  Volume 35, Issue 5, Page(s) 694–704

    Abstract: A limited set of T cell receptor (TCR) variable (V) gene segments are used to create a repertoire of TCRs that recognize all major histocompatibility complex (MHC) ligands within a species. How individual αβTCRs are constructed to specifically recognize ... ...

    Abstract A limited set of T cell receptor (TCR) variable (V) gene segments are used to create a repertoire of TCRs that recognize all major histocompatibility complex (MHC) ligands within a species. How individual αβTCRs are constructed to specifically recognize a limited set of MHC ligands is unclear. Here we have identified a role for the differential pairing of particular V gene segments in creating TCRs that recognized MHC class II ligands exclusively, or cross-reacted with classical and nonclassical MHC class I ligands. Biophysical and structural experiments indicated that TCR specificity for MHC ligands is not driven by germline-encoded pairwise interactions.Rather, identical TCRβ chains can have altered peptide-MHC (pMHC) binding modes when paired with different TCRα chains. The ability of TCR chain pairing to modify how V region residues interact with pMHC helps to explain how the same V genes are used to create TCRs specific for unique MHC ligands.
    MeSH term(s) Animals ; Cross Reactions/immunology ; Histocompatibility Antigens/chemistry ; Ligands ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Models, Molecular ; Peptides/chemistry ; Peptides/immunology ; Peptides/metabolism ; Protein Binding/immunology ; Protein Conformation ; Receptors, Antigen, T-Cell, alpha-beta/chemistry ; Receptors, Antigen, T-Cell, alpha-beta/genetics ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; Thymus Gland/immunology ; Thymus Gland/metabolism
    Chemical Substances Histocompatibility Antigens ; Ligands ; Peptides ; Receptors, Antigen, T-Cell, alpha-beta
    Language English
    Publishing date 2011-11-17
    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.2011.10.012
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 4227: Show issues Location:
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  6. 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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