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  • 1
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    A newly characterized HLA DQ beta allele associated with pemphigus vulgaris (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1988-02-26
    Beschreibung: The inheritance of particular alleles of major histocompatibility complex class II genes increases the risk for various human autoimmune diseases; however, only a small percentage of individuals having an allele associated with susceptibility develop disease. The identification of allelic variants more precisely correlated with disease susceptibility would greatly facilitate clinical screening and diagnosis. Oligonucleotide-primed gene amplification in vitro was used to determine the nucleotide sequence of a class II variant found almost exclusively in patients with the autoimmune skin disease pemphigus vulgaris. In addition to clinical implications, the disease-restricted distribution of this variant should provide insight into the molecular mechanisms underlying associations between diseases and HLA-class II genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sinha, A A -- Brautbar, C -- Szafer, F -- Friedmann, A -- Tzfoni, E -- Todd, J A -- Steinman, L -- McDevitt, H O -- New York, N.Y. -- Science. 1988 Feb 26;239(4843):1026-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Microbiology, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2894075" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alleles ; Autoimmune Diseases/*genetics/immunology ; Base Sequence ; DNA/genetics ; Gene Amplification ; Genetic Variation ; HLA-D Antigens/*genetics ; HLA-DQ Antigens/*genetics/immunology ; HLA-DR Antigens/immunology ; Humans ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Pemphigus/*genetics/immunology ; Polymorphism, Restriction Fragment Length
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    A molecular basis for MHC class II--associated autoimmunity (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1988-05-20
    Beschreibung: Class II major histocompatibility (MHC) molecules have an immunoregulatory role. These cell-surface glycoproteins present fragments of protein antigens (or peptides) to thymus-derived lymphocytes (T cells). Nucleotide sequence polymorphism in the genes that encode the class II MHC products determines the specificity of the immune response and is correlated with the development of autoimmune diseases. This study identifies certain class II polymorphic amino acid residues that are strongly associated with susceptibility to insulin-dependent diabetes mellitus, rheumatoid arthritis, and pemphigus vulgaris. These findings implicate particular class II MHC isotypes in susceptibility to each disease and suggest new prophylactic and therapeutic strategies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Todd, J A -- Acha-Orbea, H -- Bell, J I -- Chao, N -- Fronek, Z -- Jacob, C O -- McDermott, M -- Sinha, A A -- Timmerman, L -- Steinman, L -- New York, N.Y. -- Science. 1988 May 20;240(4855):1003-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Microbiology, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3368786" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Arthritis, Rheumatoid/immunology ; Autoantibodies/*genetics ; Autoimmune Diseases/*genetics ; Diabetes Mellitus, Type 1/immunology ; HLA-D Antigens/*genetics ; Humans ; Major Histocompatibility Complex ; Molecular Sequence Data ; Pemphigus/immunology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Reversal of experimental allergic encephalomyelitis with monoclonal antibody to a T-cell subset marker (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1985-01-25
    Beschreibung: Administration of a monoclonal antibody (GK1.5) that recognizes the L3T4 marker present on helper T cells prevented the development of experimental allergic encephalomyelitis (EAE) in mice. Furthermore, treatment with GK1.5 reversed EAE when the antibody was given to paralyzed animals. In vivo injection of GK1.5 selectively reduced the number of L3T4+ cells in the spleen and the lymph nodes. These results suggest that manipulation of the human equivalent of the murine L3T4+ T-cell subset with monoclonal antibodies may provide effective therapy for certain autoimmune diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Waldor, M K -- Sriram, S -- Hardy, R -- Herzenberg, L A -- Lanier, L -- Lim, M -- Steinman, L -- GM-17367/GM/NIGMS NIH HHS/ -- NS-18235/NS/NINDS NIH HHS/ -- NS-571/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Jan 25;227(4685):415-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3155574" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antibodies, Monoclonal/*therapeutic use ; Encephalomyelitis, Autoimmune, Experimental/pathology/*therapy ; Leukocyte Count ; Lymph Nodes/pathology ; Mice ; Spleen/pathology ; T-Lymphocytes, Helper-Inducer/*immunology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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    ADP-ribosyltransferase activity of pertussis toxin and immunomodulation by Bordetella pertussis (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1988-04-29
    Beschreibung: Pertussis toxin is produced by the causative agent of whooping cough, Bordetella pertussis, and is an adenosine diphosphate (ADP)-ribosyltransferase capable of covalently modifying and thereby inactivating many eukaryotic G proteins involved in cellular metabolism. The toxin is a principal determinant of virulence in whooping cough and is a primary candidate for an acellular pertussis vaccine, yet it is unclear whether the ADP-ribosyltransferase activity is required for both pathogenic and immunoprotective activities. A B. pertussis strain that produced an assembled pertussis holotoxin with only 1 percent of the ADP-ribosyltransferase activity of the native toxin was constructed and was found to be deficient in pathogenic activities associated with B. pertussis including induction of leukocytosis, potentiation of anaphylaxis, and stimulation of histamine sensitivity. Moreover, this mutant strain failed to function as an adjuvant and was less effective in protecting mice from intracerebral challenge infection. These data suggest that the ADP-ribosyltransferase activity is necessary for both pathogenicity and optimum immunoprotection. These findings bear directly on the design of a nontoxic pertussis vaccine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Black, W J -- Munoz, J J -- Peacock, M G -- Schad, P A -- Cowell, J L -- Burchall, J J -- Lim, M -- Kent, A -- Steinman, L -- Falkow, S -- AI-22462/AI/NIAID NIH HHS/ -- AI-23945/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Apr 29;240(4852):656-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Microbiology, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2896387" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): ADP Ribose Transferases ; Adjuvants, Immunologic ; Anaphylaxis/etiology ; Animals ; Antigens/immunology ; Bordetella pertussis/enzymology/genetics/*immunology ; Codon ; Drug Tolerance ; Histamine/pharmacology ; Immunization ; Leukocytosis/etiology ; Macromolecular Substances ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mutation ; Ovalbumin/immunology ; Pentosyltransferases/*metabolism ; *Pertussis Toxin ; Virulence Factors, Bordetella/genetics/immunology/*metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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