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  • 1
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    GAD, a single autoantigen for diabetes (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉von Boehmer, H -- Sarukhan, A -- New York, N.Y. -- Science. 1999 May 14;284(5417):1135, 1137.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM U373, Faculte Necker, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10366347" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoantigens/genetics/*immunology/physiology ; DNA, Antisense ; Diabetes Mellitus, Type 1/enzymology/*immunology/therapy ; Glutamate Decarboxylase/genetics/*immunology/physiology ; Humans ; Islets of Langerhans/*enzymology/immunology ; Lymphocyte Activation ; Mice ; Mice, Inbred NOD ; Mice, Transgenic ; Self Tolerance ; T-Lymphocytes/immunology ; Transgenes
    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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    Peripheral selection of the T cell repertoire (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-08
    Description: T lymphocytes undergo selection events not only in the thymus, but also after they leave the thymus and reside in the periphery. Peripheral selection was found to be dependent on T cell receptor (TCR)-ligand interactions but to differ from thymic selection with regard to specificity and mechanism. Unlike thymic selection, peripheral selection required binding of antigen to the TCR, and it induced expansion of T cell clones. Tolerance to self antigens that are restricted to the periphery occurred through the elimination of self-reactive T cells and by the clonal anergy, which was associated with down-regulation of the alpha beta TCR and CD8.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rocha, B -- von Boehmer, H -- New York, N.Y. -- Science. 1991 Mar 8;251(4998):1225-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unite INSERM U-25 CNRS UA-122, Hopital Necker, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1900951" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/immunology ; Antigens, CD8 ; Antigens, Differentiation, T-Lymphocyte/immunology ; Cells, Cultured ; Down-Regulation ; Female ; Histocompatibility Antigens Class I/immunology ; Immunotherapy, Adoptive ; Male ; Mice ; Mice, Nude ; Receptors, Antigen, T-Cell/*physiology ; T-Lymphocytes/*immunology ; Thymectomy ; Thymus Gland/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Self-nonself discrimination by T cells (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-15
    Description: The alpha beta T cell receptor (TCR) recognizes antigens that are presented by major histocompatibility complex (MHC)-encoded cell surface molecules by binding to both the antigen and the MHC molecules. Discrimination of self from nonself antigens and MHC molecules is achieved by negative and positive selection of T cells in the thymus: potentially harmful T cells with receptors that bind to self antigens plus self MHC molecules are deleted before they can mount immune responses. In contrast, the maturation of useful T cells with receptors that bind foreign antigens plus self MHC molecules requires the binding of their receptor to MHC molecules on thymic epithelium in the absence of foreign antigen. The binding of the TCR to either class I or class II MHC molecules directs differentiation of the selected cells into either CD4-8+ (killer) or CD4+8- (helper) T cells, respectively.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉von Boehmer, H -- Kisielow, P -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1369-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basel Institute for Immunology, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1972594" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD4-Positive T-Lymphocytes/immunology ; Cell Differentiation ; Cell Survival ; Female ; H-2 Antigens/immunology ; Histocompatibility Antigens/immunology ; *Immune Tolerance ; Killer Cells, Natural/immunology ; Male ; Mice ; Mice, Transgenic ; Phenotype ; Receptors, Antigen, T-Cell/genetics/immunology ; T-Lymphocytes/*immunology ; T-Lymphocytes, Helper-Inducer/immunology ; T-Lymphocytes, Regulatory/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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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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  • 5
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    Immunology. Thoracic thymus, exclusive no longer (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉von Boehmer, Harald -- New York, N.Y. -- Science. 2006 Apr 14;312(5771):206-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Harvard Medical School, Dana-Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA. harald_von_boehmer@dfci.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16614204" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Lymphopoiesis ; Mice ; *Neck ; Receptors, Antigen, T-Cell ; T-Lymphocytes/*immunology/physiology ; Thymus Gland/embryology/growth & development/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    MHC class I expression in mice lacking the proteasome subunit LMP-7 (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-08-26
    Description: Proteasomes degrade endogenous proteins. Two subunits, LMP-2 and LMP-7, are encoded in a region of the major histocompatibility complex (MHC) that is critical for class I-restricted antigen presentation. Mice with a targeted deletion of the gene encoding LMP-7 have reduced levels of MHC class I cell-surface expression and present the endogenous antigen HY inefficiently; addition of peptides to splenocytes deficient in LMP-7 restores wild-type class I expression levels. This demonstrates the involvement of LMP-7 in the MHC class I presentation pathway and suggests that LMP-7 functions as an integral part of the peptide supply machinery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fehling, H J -- Swat, W -- Laplace, C -- Kuhn, R -- Rajewsky, K -- Muller, U -- von Boehmer, H -- New York, N.Y. -- Science. 1994 Aug 26;265(5176):1234-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basel Institute for Immunology, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8066463" target="_blank"〉PubMed〈/a〉
    Keywords: *ATP-Binding Cassette Transporters ; Amino Acid Sequence ; Animals ; Antigen Presentation ; Antigen-Presenting Cells/immunology ; Base Sequence ; Carrier Proteins/genetics ; *Cysteine Endopeptidases ; Female ; Gene Deletion ; H-2 Antigens/*biosynthesis/immunology ; H-Y Antigen/immunology ; Lymphocytes/immunology ; Male ; Mice ; Mice, Knockout ; Molecular Sequence Data ; *Multienzyme Complexes ; Proteasome Endopeptidase Complex ; Proteins/genetics/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Analysis and expression of a cloned pre-T cell receptor gene (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-18
    Description: The T cell antigen receptor (TCR) beta chain regulates early T cell development in the absence of the TCR alpha chain. The developmentally controlled gene described here encodes the pre-TCR alpha (pT alpha) chain, which covalently associates with TCR beta and with the CD3 proteins forms a pre-TCR complex that transduces signals in immature thymocytes. Unlike the lambda 5 pre-B cell receptor protein, the pT alpha chain is a type I transmembrane protein whose cytoplasmic tail contains two potential phosphorylation sites and a Src homology 3 (SH3)-domain binding sequence. Pre-TCR alpha transfection experiments indicated that surface expression of the pre-TCR is controlled by additional developmentally regulated proteins. Identification of the pT alpha gene represents an essential step in the structure-function analysis of the pre-TCR complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saint-Ruf, C -- Ungewiss, K -- Groettrup, M -- Bruno, L -- Fehling, H J -- von Boehmer, H -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1208-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unite INSERM 373, Institut Necker, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973703" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD3/metabolism ; Base Sequence ; Cell Line ; *Cloning, Molecular ; DNA, Complementary/genetics ; *Gene Expression Regulation, Developmental ; Gene Rearrangement ; Membrane Glycoproteins/chemistry/*genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Open Reading Frames ; Phosphorylation ; Polymerase Chain Reaction ; Rabbits ; Receptors, Antigen, T-Cell, alpha-beta/chemistry/*genetics/metabolism ; Signal Transduction ; T-Lymphocytes/*immunology ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
    Electronic Resource
    Electronic Resource
    Control of T cell development by the αsz T cell receptor for antigen
    Amsterdam : Elsevier
    Cell Differentiation and Development 27 (1989), S. 63 
    Details
    ISSN: 0922-3371
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0922-3371(89)90216-5
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  • 9
    Electronic Resource
    Electronic Resource
    Cryopreservation of cytotoxic T-cell clones and their targets
    Amsterdam : Elsevier
    Cryobiology 17 (1980), S. 597 
    Details
    ISSN: 0011-2240
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0011-2240(80)90087-5
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  • 10
    Electronic Resource
    Electronic Resource
    Preservation of cloned T cells cytotoxic for male-antigen-bearing target cells
    Amsterdam : Elsevier
    Cryobiology 16 (1979), S. 607 
    Details
    ISSN: 0011-2240
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0011-2240(79)90155-X
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