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  • 1
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    Selection for survival? (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Benoist, C -- Mathis, D -- New York, N.Y. -- Science. 1997 Jun 27;276(5321):2000-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire (INSERM, CNRS, ULP), 1 rue Laurent Fries, 6704 Illkirch, C.U. de Strasbourg, France. cb@titus.u-strasbg.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9221508" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD8-Positive T-Lymphocytes/cytology/*immunology ; Cell Division ; Cell Survival ; Female ; H-2 Antigens/immunology ; H-Y Antigen/immunology ; Histocompatibility Antigen H-2D ; Humans ; *Immunologic Memory ; Lymphocyte Activation ; Male ; Mice ; Mice, Transgenic ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocyte Subsets/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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  • 2
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    Projection of an immunological self shadow within the thymus by the aire protein (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-10-12
    Description: Humans expressing a defective form of the transcription factor AIRE (autoimmune regulator) develop multiorgan autoimmune disease. We used aire- deficient mice to test the hypothesis that this transcription factor regulates autoimmunity by promoting the ectopic expression of peripheral tissue- restricted antigens in medullary epithelial cells of the thymus. This hypothesis proved correct. The mutant animals exhibited a defined profile of autoimmune diseases that depended on the absence of aire in stromal cells of the thymus. Aire-deficient thymic medullary epithelial cells showed a specific reduction in ectopic transcription of genes encoding peripheral antigens. These findings highlight the importance of thymically imposed "central" tolerance in controlling autoimmunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, Mark S -- Venanzi, Emily S -- Klein, Ludger -- Chen, Zhibin -- Berzins, Stuart P -- Turley, Shannon J -- von Boehmer, Harald -- Bronson, Roderick -- Dierich, Andree -- Benoist, Christophe -- Mathis, Diane -- 2 P30 DK36836-16/DK/NIDDK NIH HHS/ -- 2T32 DK07260-26/DK/NIDDK NIH HHS/ -- KO8-DK59958-01A1/DK/NIDDK NIH HHS/ -- R01 DK60027-01/DK/NIDDK NIH HHS/ -- T32CA70083-05/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2002 Nov 15;298(5597):1395-401. Epub 2002 Oct 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section on Immunology and Immunogenetics, Joslin Diabetes Center; Department of Medicine, Brigham and Women's Hospital; Harvard Medical School, 1 Joslin Place, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12376594" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Autoantibodies/analysis/blood ; Autoantigens/biosynthesis/genetics ; Autoimmune Diseases/genetics/immunology/metabolism ; Autoimmunity ; Epithelial Cells/physiology ; Female ; Gene Expression Profiling ; Gene Expression Regulation ; Gene Targeting ; Humans ; Lymphocytes/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Polyendocrinopathies, Autoimmune/genetics/immunology/metabolism ; Radiation Chimera ; Reverse Transcriptase Polymerase Chain Reaction ; *Self Tolerance ; Stromal Cells/immunology/metabolism ; T-Lymphocytes/*immunology ; Thymus Gland/cytology/*immunology/*metabolism ; Transcription Factors/genetics/*metabolism
    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)
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  • 4
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    Islet recovery and reversal of murine type 1 diabetes in the absence of any infused spleen cell contribution (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-03-25
    Description: A cure for type 1 diabetes will probably require the provision or elicitation of new pancreatic islet beta cells as well as the reestablishment of immunological tolerance. A 2003 study reported achievement of both advances in the NOD mouse model by coupling injection of Freund's complete adjuvant with infusion of allogeneic spleen cells. It was concluded that the adjuvant eliminated anti-islet autoimmunity and the donor splenocytes differentiated into insulin-producing (presumably beta) cells, culminating in islet regeneration. Here, we provide data indicating that the recovered islets were all of host origin, reflecting that the diabetic NOD mice actually retain substantial beta cell mass, which can be rejuvenated/regenerated to reverse disease upon adjuvant-dependent dampening of autoimmunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nishio, Junko -- Gaglia, Jason L -- Turvey, Stuart E -- Campbell, Christopher -- Benoist, Christophe -- Mathis, Diane -- T32 CA09382/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2006 Mar 24;311(5768):1775-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section on Immunology and Immunogenetics, Joslin Diabetes Center, and Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, and Harvard Stem Cell Institute, 1 Joslin Place, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16556845" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/immunology ; Autoimmunity ; Blood Glucose/analysis ; Cell Differentiation ; *Cell Transplantation ; Combined Modality Therapy ; Diabetes Mellitus, Type 1/immunology/pathology/*therapy ; Female ; Freund's Adjuvant/*therapeutic use ; Insulin-Secreting Cells/*cytology ; Islets of Langerhans/*cytology/pathology ; *Islets of Langerhans Transplantation ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Polymorphism, Single Nucleotide ; Regeneration ; Spleen/*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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