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  • Animals  (2)
  • *Gene Expression Profiling  (1)
  • Controlled Clinical Trials as Topic  (1)
  • Encephalomyelitis, Autoimmune,  (1)
  • 2010-2014
  • 2000-2004  (3)
  • 1
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    American Association for the Advancement of Science (AAAS)
    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
    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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    American Association for the Advancement of Science (AAAS)
    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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