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  • 1
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    Altered peptide ligands and MS treatment (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-06-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Conlon, Paul -- Steinman, Lawrence -- New York, N.Y. -- Science. 2002 Jun 7;296(5574):1801-2; author reply 1801-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12053936" target="_blank"〉PubMed〈/a〉
    Keywords: Clinical Trials as Topic ; Controlled Clinical Trials as Topic ; Double-Blind Method ; Humans ; Ligands ; Multicenter Studies as Topic ; Multiple Sclerosis/*drug therapy ; Peptide Fragments/*adverse effects/*therapeutic use
    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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  • 2
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    The influence of the proinflammatory cytokine, osteopontin, on autoimmune demyelinating disease (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-11-27
    Description: Multiple sclerosis is a demyelinating disease, characterized by inflammation in the brain and spinal cord, possibly due to autoimmunity. Large-scale sequencing of cDNA libraries, derived from plaques dissected from brains of patients with multiple sclerosis (MS), indicated an abundance of transcripts for osteopontin (OPN). Microarray analysis of spinal cords from rats paralyzed by experimental autoimmune encephalomyelitis (EAE), a model of MS, also revealed increased OPN transcripts. Osteopontin-deficient mice were resistant to progressive EAE and had frequent remissions, and myelin-reactive T cells in OPN-/- mice produced more interleukin 10 and less interferon-gamma than in OPN+/+ mice. Osteopontin thus appears to regulate T helper cell-1 (TH1)-mediated demyelinating disease, and it may offer a potential target in blocking development of progressive MS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chabas, D -- Baranzini, S E -- Mitchell, D -- Bernard, C C -- Rittling, S R -- Denhardt, D T -- Sobel, R A -- Lock, C -- Karpuj, M -- Pedotti, R -- Heller, R -- Oksenberg, J R -- Steinman, L -- New York, N.Y. -- Science. 2001 Nov 23;294(5547):1731-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neurological Sciences, Beckman Center for Molecular Medicine, B002, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11721059" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Encephalomyelitis, Autoimmune, ; Experimental/genetics/immunology/metabolism/pathology ; Expressed Sequence Tags ; Gene Deletion ; *Gene Expression Profiling ; Gene Library ; Humans ; Inflammation/genetics/immunology/metabolism/pathology ; Interferon-gamma/genetics/metabolism ; Interleukin-10/genetics/metabolism ; Lymphocyte Activation ; Mice ; Mice, Knockout ; Multiple Sclerosis/*genetics/immunology/*metabolism/pathology ; Oligonucleotide Array Sequence Analysis ; Osteopontin ; RNA, Messenger/genetics/metabolism ; Rats ; Sialoglycoproteins/deficiency/genetics/*metabolism ; Spinal Cord/metabolism ; Th1 Cells/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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    A newly characterized HLA DQ beta allele associated with pemphigus vulgaris (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-02-26
    Description: 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〉
    Keywords: 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
    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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    A molecular basis for MHC class II--associated autoimmunity (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-05-20
    Description: 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〉
    Keywords: 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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Predominant expression of T cell receptor V alpha 7 in tumor-infiltrating lymphocytes of uveal melanoma (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-10
    Description: Expression of T cell receptor (TCR) V alpha genes in tumor-infiltrating lymphocytes (TILs) within intraocular melanoma was studied. Primers for 18 different human TCR V alpha families were used to analyze TCR V alpha-C alpha gene rearrangements in TIL in these melanomas obtained at surgery. A limited number of TCR V alpha genes were expressed and rearranged in these tumors, and TILs expressing V alpha 7 were found in seven of eight of these uveal melanomas. TCR gene usage is also restricted in experimental autoimmune disease, in T cells within organs like skin and other epithelial tissues, and in the brain of patients with multiple sclerosis (MS). The restricted usage of TCR genes in TIL may indicate that a specific antigen in these melanomas is targeted.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nitta, T -- Oksenberg, J R -- Rao, N A -- Steinman, L -- New York, N.Y. -- Science. 1990 Aug 10;249(4969):672-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Stanford University Medical Center, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2382141" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; DNA, Neoplasm/genetics ; Humans ; Lymphocytes/*immunology ; Melanoma/genetics/*immunology ; Molecular Sequence Data ; Multigene Family ; Oligonucleotide Probes ; Polymerase Chain Reaction ; RNA, Messenger/genetics ; Receptors, Antigen, T-Cell/*genetics ; Uveal Neoplasms/genetics/*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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    Immune therapy for autoimmune diseases (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-07-13
    Description: Our increasing understanding of the pathophysiology of autoimmune disease has revealed a number of checkpoints that can be targeted with immune therapy, including key mediators of lymphocyte adhesion and migration, destructive cytokines involved in tissue damage, and the complex of molecules critical in the presentation of self-antigen and the activation of autoaggressive T lymphocytes. In many organ-specific autoimmune diseases, the identity of the molecules attacked by T cells and autoantibodies is known and attempts are under way to tolerize the immune system with a high level of specificity to these targets.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steinman, Lawrence -- New York, N.Y. -- Science. 2004 Jul 9;305(5681):212-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurological Sciences and Neurology, and Interdepartmental Program in Immunology, Stanford University, Stanford, CA 94305, USA. steinman@stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15247472" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; Autoantibodies/immunology ; Autoantigens/immunology ; Autoimmune Diseases/*therapy ; Clinical Trials as Topic ; Cytokines/antagonists & inhibitors/immunology/therapeutic use ; Epitopes/immunology ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use ; Immunosuppressive Agents/therapeutic use ; *Immunotherapy ; Receptors, Cytokine/antagonists & inhibitors/immunology ; Receptors, Lymphocyte Homing/antagonists & inhibitors/immunology/metabolism ; Self Tolerance ; T-Lymphocytes/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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  • 7
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    Treatment of autoimmune neuroinflammation with a synthetic tryptophan metabolite (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-11-08
    Description: Local catabolism of the amino acid tryptophan (Trp) by indoleamine 2,3-dioxygenase (IDO) is considered an important mechanism of regulating T cell immunity. We show that IDO transcription was increased when myelin-specific T cells were stimulated with tolerogenic altered self-peptides. Catabolites of Trp suppressed proliferation of myelin-specific T cells and inhibited production of proinflammatory T helper-1 (T(H)1) cytokines. N-(3,4,-Dimethoxycinnamoyl) anthranilic acid (3,4-DAA), an orally active synthetic derivative of the Trp metabolite anthranilic acid, reversed paralysis in mice with experimental autoimmune encephalomyelitis, a model of multiple sclerosis (MS). Trp catabolites and their derivatives offer a new strategy for treating T(H)1-mediated autoimmune diseases such as MS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Platten, Michael -- Ho, Peggy P -- Youssef, Sawsan -- Fontoura, Paulo -- Garren, Hideki -- Hur, Eun Mi -- Gupta, Rohit -- Lee, Lowen Y -- Kidd, Brian A -- Robinson, William H -- Sobel, Raymond A -- Selley, Michael L -- Steinman, Lawrence -- New York, N.Y. -- Science. 2005 Nov 4;310(5749):850-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neurological Sciences, Beckman Center for Molecular Medicine, Stanford University, Stanford, CA 94305, USA. michael.platten@uni-tuebingen.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16272121" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Anti-Inflammatory Agents, Non-Steroidal/administration & ; dosage/pharmacology/*therapeutic use ; Antigen-Presenting Cells/drug effects/immunology ; Brain/pathology ; Cell Line ; Cytokines/biosynthesis ; Disease Models, Animal ; Encephalomyelitis, Autoimmune, Experimental/*drug therapy/immunology ; Female ; Histocompatibility Antigens Class II/immunology/metabolism ; Immune Tolerance ; Immunosuppressive Agents/pharmacology/therapeutic use ; Indoleamine-Pyrrole 2,3,-Dioxygenase/genetics/metabolism ; Interferon-gamma/immunology ; Lymphocyte Activation ; Mice ; Mice, Transgenic ; Microglia/drug effects/immunology ; Multiple Sclerosis/drug therapy/immunology/pathology ; Myelin Proteins/immunology ; Signal Transduction ; Spinal Cord/pathology ; T-Lymphocytes/immunology ; Th1 Cells/immunology ; Th2 Cells/immunology ; Tryptophan/*metabolism ; ortho-Aminobenzoates/administration & dosage/pharmacology/*therapeutic use
    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
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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
    Publication Date: 1985-01-25
    Description: 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〉
    Keywords: 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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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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
    Publication Date: 1988-04-29
    Description: 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〉
    Keywords: 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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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