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  • 1
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    T cells against a bacterial heat shock protein recognize stressed macrophages (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-09-08
    Description: Heat shock proteins are evolutionarily highly conserved polypeptides that are produced under a variety of stress conditions to preserve cellular functions. A major antigen of tubercle bacilli of 65 kilodaltons is a heat shock protein that has significant sequence similarity and cross-reactivity with antigens of various other microbes. Monoclonal antibodies against this common bacterial heat shock protein were used to identify a molecule of similar size in murine macrophages. Macrophages subjected to various stress stimuli including interferon-gamma activation and viral infection were recognized by class I-restricted CD8 T cells raised against the bacterial heat shock protein. These data suggest that heat shock proteins are processed in stressed host cells and that epitopes shared by heat shock proteins of bacterial and host origin are presented in the context of class I molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koga, T -- Wand-Wurttenberger, A -- DeBruyn, J -- Munk, M E -- Schoel, B -- Kaufmann, S H -- New York, N.Y. -- Science. 1989 Sep 8;245(4922):1112-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Microbiology and Immunology, University of Ulm, Federal Republic of Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2788923" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Bacterial/physiology ; Antibodies, Monoclonal/physiology ; Antigens, Differentiation, T-Lymphocyte/immunology ; Bacterial Proteins/*immunology/pharmacology ; Binding, Competitive ; Cross Reactions ; Cytotoxicity, Immunologic ; Heat-Shock Proteins/*immunology/pharmacology ; Macrophages/drug effects/*immunology ; Mice ; Mice, Inbred C57BL ; T-Lymphocytes, Cytotoxic/*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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    Therapeutic silencing of microRNA-122 in primates with chronic hepatitis C virus infection (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: The liver-expressed microRNA-122 (miR-122) is essential for hepatitis C virus (HCV) RNA accumulation in cultured liver cells, but its potential as a target for antiviral intervention has not been assessed. We found that treatment of chronically infected chimpanzees with a locked nucleic acid (LNA)-modified oligonucleotide (SPC3649) complementary to miR-122 leads to long-lasting suppression of HCV viremia, with no evidence of viral resistance or side effects in the treated animals. Furthermore, transcriptome and histological analyses of liver biopsies demonstrated derepression of target mRNAs with miR-122 seed sites, down-regulation of interferon-regulated genes, and improvement of HCV-induced liver pathology. The prolonged virological response to SPC3649 treatment without HCV rebound holds promise of a new antiviral therapy with a high barrier to resistance.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3436126/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3436126/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lanford, Robert E -- Hildebrandt-Eriksen, Elisabeth S -- Petri, Andreas -- Persson, Robert -- Lindow, Morten -- Munk, Martin E -- Kauppinen, Sakari -- Orum, Henrik -- C06 RR 12087/RR/NCRR NIH HHS/ -- C06 RR012087/RR/NCRR NIH HHS/ -- C06 RR012087-01/RR/NCRR NIH HHS/ -- P51 RR013986/RR/NCRR NIH HHS/ -- P51 RR13986/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2010 Jan 8;327(5962):198-201. doi: 10.1126/science.1178178. Epub 2009 Dec 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Virology and Immunology and Southwest National Primate Research Center, Southwest Foundation for Biomedical Research, San Antonio, TX 78227, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965718" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antiviral Agents/adverse effects/blood/*therapeutic use ; Chemokine CXCL10/blood ; Cholesterol/blood ; Disease Models, Animal ; Drug Evaluation, Preclinical ; Drug Resistance, Viral ; Female ; Gene Expression Profiling ; Gene Expression Regulation ; Hepacivirus/drug effects/genetics/isolation & purification/physiology ; Hepatitis C, Chronic/*drug therapy/genetics/virology ; Interferons/metabolism ; Liver/metabolism/virology ; Male ; MicroRNAs/*antagonists & inhibitors/genetics/metabolism ; *Pan troglodytes ; Phosphorothioate Oligonucleotides/adverse effects/blood/*therapeutic use ; RNA, Messenger/genetics/metabolism ; RNA, Viral/metabolism ; Viral Load ; Viremia/drug therapy
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
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