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  • T-Lymphocytes/*immunology  (2)
  • *Cytotoxicity, Immunologic  (1)
  • Mice, Knockout
  • 1995-1999  (3)
  • 1
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    Arthritis provoked by linked T and B cell recognition of a glycolytic enzyme (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-27
    Description: The hallmark of rheumatoid arthritis (RA) is specific destruction of the synovial joints. In a mouse line that spontaneously develops a disorder with many of the features of human RA, disease is initiated by T cell recognition of a ubiquitously expressed self-antigen; once initiated, pathology is driven almost entirely by immunoglobulins. In this study, the target of both the initiating T cells and pathogenic immunoglobulins was identified as glucose-6-phosphate isomerase, a glycolytic enzyme. Thus, some forms of RA or related arthritides may develop by a mechanism fundamentally different from the currently popular paradigm of a joint-specific T cell response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsumoto, I -- Staub, A -- Benoist, C -- Mathis, D -- New York, N.Y. -- Science. 1999 Nov 26;286(5445):1732-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire (CNRS/INSERM/ULP), BP 163, 67404 Illkirch, C.U. de Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10576739" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; Antigen-Antibody Complex/immunology/metabolism ; Arthritis, Rheumatoid/*immunology ; Autoantibodies/*immunology ; Autoantigens/*immunology ; B-Lymphocytes/*immunology ; Cross Reactions ; Disease Models, Animal ; Glucose-6-Phosphate Isomerase/chemistry/*immunology ; Humans ; Immunoglobulins/immunology ; Joints/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Mice, Transgenic ; Recombinant Fusion Proteins/immunology ; T-Lymphocytes/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Positive selection of T cells induced by viral delivery of neopeptides to the thymus (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-31
    Description: The relation between an antigenic peptide that can stimulate a mature T cell and the natural peptide that promoted selection of this cell in the thymus is still unknown. An experimental system was devised to address this issue in vivo-mice expressing neopeptides in thymic stromal cells after adenovirus-mediated delivery of invariant chain-peptide fusion proteins. In this system, selection of T cells capable of responding to a given antigenic peptide could be promoted by the peptide itself, by closely related analogs lacking agonist and antagonist activity, or by ostensibly unrelated peptides. However, the precise repertoire of T cells selected was dictated by the particular neopeptide expressed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakano, N -- Rooke, R -- Benoist, C -- Mathis, D -- New York, N.Y. -- Science. 1997 Jan 31;275(5300):678-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire (INSERM, CNRS, Universite Louis Pasteur), 1 rue Laurent Fries, 67404 Illkirch, C.U. de Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9005856" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Amino Acid Sequence ; Animals ; Antigen-Presenting Cells/immunology ; Antigens, Differentiation, B-Lymphocyte/genetics ; Cells, Cultured ; Cloning, Molecular ; Cross Reactions ; Cytochrome c Group/immunology ; DNA, Complementary/genetics ; Genetic Vectors ; Histocompatibility Antigens Class II/genetics ; Hybridomas ; Interleukin-2/biosynthesis ; *Lymphocyte Activation ; Mice ; Molecular Sequence Data ; Peptides/chemistry/*immunology ; Receptors, Antigen, T-Cell/*immunology ; Recombinant Fusion Proteins ; T-Lymphocytes/*immunology ; Thymus Gland/cytology/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Independent modes of natural killing distinguished in mice lacking Lag3 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-04-19
    Description: The LAG3 protein has several features in common with CD4, suggesting that it may be important in controlling T cell reactivity. However, mice with a Lag3 null mutation have now been shown to exhibit a defect in the natural killer cell, rather than the T cell, compartment. Killing of certain tumor targets by natural killer cells from these mice was inhibited or even abolished, whereas lysis of cells displaying major histocompatibility complex class I disparities remained intact. It appears that LAG3 is a receptor or coreceptor that defines different modes of natural killing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyazaki, T -- Dierich, A -- Benoist, C -- Mathis, D -- New York, N.Y. -- Science. 1996 Apr 19;272(5260):405-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire (INSERM, CNRS, ULP), Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8602528" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigens, CD ; B-Lymphocytes/immunology ; Base Sequence ; *Cytotoxicity, Immunologic ; Female ; Histocompatibility Antigens Class I/immunology ; Killer Cells, Natural/*immunology ; Male ; Membrane Proteins/genetics/*physiology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutation ; Phenotype ; T-Lymphocytes/immunology ; Tumor Cells, Cultured ; beta 2-Microglobulin/deficiency/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
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