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  • 1
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    Host defense mechanisms triggered by microbial lipoproteins through toll-like receptors (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: The generation of cell-mediated immunity against many infectious pathogens involves the production of interleukin-12 (IL-12), a key signal of the innate immune system. Yet, for many pathogens, the molecules that induce IL-12 production by macrophages and the mechanisms by which they do so remain undefined. Here it is shown that microbial lipoproteins are potent stimulators of IL-12 production by human macrophages, and that induction is mediated by Toll-like receptors (TLRs). Several lipoproteins stimulated TLR-dependent transcription of inducible nitric oxide synthase and the production of nitric oxide, a powerful microbicidal pathway. Activation of TLRs by microbial lipoproteins may initiate innate defense mechanisms against infectious pathogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brightbill, H D -- Libraty, D H -- Krutzik, S R -- Yang, R B -- Belisle, J T -- Bleharski, J R -- Maitland, M -- Norgard, M V -- Plevy, S E -- Smale, S T -- Brennan, P J -- Bloom, B R -- Godowski, P J -- Modlin, R L -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):732-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Howard Hughes Medical Institute, University of California Los Angeles School of Medicine, Los Anges, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426995" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Bacterial/chemistry/*immunology/metabolism ; Cell Line ; *Drosophila Proteins ; Gene Expression Regulation ; Humans ; Interleukin-12/*biosynthesis/genetics ; Lipopolysaccharides/immunology ; Lipoproteins/chemistry/*immunology/metabolism ; Macrophages/*immunology/metabolism ; Membrane Glycoproteins/*metabolism ; Mice ; Monocytes/*immunology/metabolism ; Mycobacterium tuberculosis/*immunology ; NF-kappa B/biosynthesis ; Nitric Oxide Synthase/genetics ; Nitric Oxide Synthase Type II ; Promoter Regions, Genetic ; Receptors, Cell Surface/*metabolism ; Signal Transduction ; Toll-Like Receptors ; Transcription, Genetic ; Transfection ; Tumor Cells, Cultured
    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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    Induction of direct antimicrobial activity through mammalian toll-like receptors (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-02-27
    Description: The mammalian innate immune system retains from Drosophila a family of homologous Toll-like receptors (TLRs) that mediate responses to microbial ligands. Here, we show that TLR2 activation leads to killing of intracellular Mycobacterium tuberculosis in both mouse and human macrophages, through distinct mechanisms. In mouse macrophages, bacterial lipoprotein activation of TLR2 leads to a nitric oxide-dependent killing of intracellular tubercle bacilli, but in human monocytes and alveolar macrophages, this pathway was nitric oxide-independent. Thus, mammalian TLRs respond (as Drosophila Toll receptors do) to microbial ligands and also have the ability to activate antimicrobial effector pathways at the site of infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thoma-Uszynski, S -- Stenger, S -- Takeuchi, O -- Ochoa, M T -- Engele, M -- Sieling, P A -- Barnes, P F -- Rollinghoff, M -- Bolcskei, P L -- Wagner, M -- Akira, S -- Norgard, M V -- Belisle, J T -- Godowski, P J -- Bloom, B R -- Modlin, R L -- AI 07118/AI/NIAID NIH HHS/ -- AI 22553/AI/NIAID NIH HHS/ -- AI 47868/AI/NIAID NIH HHS/ -- AR 40312/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2001 Feb 23;291(5508):1544-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Dermatology, Department of Microbiology and Immunology and Molecular Biology Institute, UCLA School of Medicine, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11222859" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins/immunology ; Cell Line ; Cells, Cultured ; *Drosophila Proteins ; Humans ; Interferon-gamma/immunology/pharmacology ; Ligands ; Lipoproteins/*immunology ; Macrophage Activation ; Macrophages/immunology/metabolism/*microbiology ; Macrophages, Alveolar/immunology/metabolism/microbiology ; Macrophages, Peritoneal/immunology/metabolism/microbiology ; Membrane Glycoproteins/*metabolism ; Mice ; Monocytes/immunology/metabolism/*microbiology ; Mycobacterium tuberculosis/growth & development/*immunology ; Nitric Oxide/*metabolism ; Nitric Oxide Synthase/antagonists & inhibitors/metabolism ; Nitric Oxide Synthase Type II ; Receptors, Cell Surface/*metabolism ; Signal Transduction ; Toll-Like Receptor 2 ; Toll-Like Receptors ; Tumor Necrosis Factor-alpha/immunology/pharmacology
    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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    Immunology. Chip shots--will functional genomics get functional? (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-10-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Modlin, R L -- Bloom, B R -- New York, N.Y. -- Science. 2001 Oct 26;294(5543):799-801.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Dermatology and Department of Microbiology and Immunology, UCLA School of Medicine, Los Angeles, CA 90095, USA. rmodlin@mednet.ucla.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11679655" target="_blank"〉PubMed〈/a〉
    Keywords: Candida albicans/immunology ; Cells, Cultured ; Dendritic Cells/*immunology/*metabolism ; Escherichia coli/immunology ; *Gene Expression Profiling ; *Gene Expression Regulation ; Genomics ; Humans ; Immunity, Innate ; Influenza A virus/immunology ; Ligands ; Lipopolysaccharides/immunology ; Mannans/immunology ; Oligonucleotide Array Sequence Analysis ; RNA, Double-Stranded/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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    An antimicrobial activity of cytolytic T cells mediated by granulysin (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-02
    Description: Cytolytic T lymphocytes (CTLs) kill intracellular pathogens by a granule-dependent mechanism. Granulysin, a protein found in granules of CTLs, reduced the viability of a broad spectrum of pathogenic bacteria, fungi, and parasites in vitro. Granulysin directly killed extracellular Mycobacterium tuberculosis, altering the membrane integrity of the bacillus, and, in combination with perforin, decreased the viability of intracellular M. tuberculosis. The ability of CTLs to kill intracellular M. tuberculosis was dependent on the presence of granulysin in cytotoxic granules, defining a mechanism by which T cells directly contribute to immunity against intracellular pathogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stenger, S -- Hanson, D A -- Teitelbaum, R -- Dewan, P -- Niazi, K R -- Froelich, C J -- Ganz, T -- Thoma-Uszynski, S -- Melian, A -- Bogdan, C -- Porcelli, S A -- Bloom, B R -- Krensky, A M -- Modlin, R L -- New York, N.Y. -- Science. 1998 Oct 2;282(5386):121-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, UCLA School of Medicine, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9756476" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Differentiation, T-Lymphocyte/analysis/*immunology/pharmacology ; Cell Line ; Cell Membrane/ultrastructure ; Cells, Cultured ; Cytoplasmic Granules/immunology ; *Cytotoxicity, Immunologic ; Humans ; Macrophages/immunology/microbiology ; Membrane Glycoproteins/immunology/pharmacology ; Microscopy, Confocal ; Microscopy, Electron, Scanning ; Mycobacterium tuberculosis/*immunology/physiology/ultrastructure ; Perforin ; Pore Forming Cytotoxic Proteins ; Recombinant Proteins/pharmacology ; 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
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  • 5
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    Investing in the World Health Organization (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bloom, B R -- Bloom, D E -- Cohen, J E -- Sachs, J D -- New York, N.Y. -- Science. 1999 May 7;284(5416):911.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10357669" target="_blank"〉PubMed〈/a〉
    Keywords: Budgets ; Financing, Government ; United States ; World Health Organization/*economics/organization & administration
    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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    Chips, infections, and national security (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-11-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Modlin, R L -- Bloom, B R -- New York, N.Y. -- Science. 2001 Nov 9;294(5545):1279.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11702789" target="_blank"〉PubMed〈/a〉
    Keywords: *Bioterrorism ; Gene Expression ; Humans ; Infection/*diagnosis ; *Oligonucleotide Array Sequence Analysis ; Sensitivity and Specificity
    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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    The highest attainable standard: ethical issues in AIDS vaccines (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-01-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bloom, B R -- New York, N.Y. -- Science. 1998 Jan 9;279(5348):186-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Albert Einstein College of Medicine, Bronx, NY 10461, USA. bloom@aecom.yu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9446225" target="_blank"〉PubMed〈/a〉
    Keywords: *AIDS Vaccines ; Anti-HIV Agents/therapeutic use ; Clinical Trials as Topic/*standards ; Codes of Ethics ; Controlled Clinical Trials as Topic/*standards ; Developed Countries ; Developing Countries ; Ethical Review ; *Ethics, Medical ; HIV Infections/drug therapy/*prevention & control/transmission ; Human Experimentation ; Humans ; *Internationality ; Placebos ; Practice Guidelines as Topic ; *Therapeutic Human Experimentation ; United Nations
    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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    Differing lymphokine profiles of functional subsets of human CD4 and CD8 T cell clones (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-11
    Description: Functional subsets of human T cells were delineated by analyzing patterns of lymphokines produced by clones from individuals with leprosy and by T cell clones of known function. CD4 clones from individuals with strong cell-mediated immunity produced predominantly interferon-gamma, whereas those clones that enhanced antibody formation produced interleukin-4. CD8 cytotoxic T cells secreted interferon-gamma. Interleukin-4 was produced by CD8 T suppressor clones from immunologically unresponsive individuals with leprosy and was found to be necessary for suppression in vitro. Both the classic reciprocal relation between antibody formation and cell-mediated immunity and resistance or susceptibility to certain infections may be explained by T cell subsets differing in patterns of lymphokine production.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Salgame, P -- Abrams, J S -- Clayberger, C -- Goldstein, H -- Convit, J -- Modlin, R L -- Bloom, B R -- AI-07118/AI/NIAID NIH HHS/ -- AI-20111/AI/NIAID NIH HHS/ -- AI-26491/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1991 Oct 11;254(5029):279-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Albert Einstein College of Medicine, New York, NY 10461.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1681588" target="_blank"〉PubMed〈/a〉
    Keywords: Antibody Formation ; *Antigens, CD4 ; *Antigens, CD8 ; CD4-Positive T-Lymphocytes/secretion ; Clone Cells ; Humans ; Interferon-gamma/secretion ; Interleukin-4/secretion ; Interleukins/secretion ; Leprosy/immunology ; Lymphokines/*secretion ; T-Lymphocyte Subsets/*secretion ; T-Lymphocytes/secretion
    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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    Tuberculosis: commentary on a reemergent killer (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-21
    Description: Tuberculosis remains the leading cause of death in the world from a single infectious disease, although there is little knowledge of the mechanisms of its pathogenesis and protection from it. After a century of decline in the United States, tuberculosis is increasing, and strains resistant to multiple antibiotics have emerged. This excess of cases is attributable to changes in the social structure in cities, the human immunodeficiency virus epidemic, and a failure in certain major cities to improve public treatment programs. The economic costs of not adequately addressing the problem of tuberculosis in this country are estimated from an epidemiological model.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bloom, B R -- Murray, C J -- New York, N.Y. -- Science. 1992 Aug 21;257(5073):1055-64.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Albert Einstein College of Medicine, Bronx, NY 10461.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1509256" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/complications ; Animals ; Antibiotics, Antitubercular/pharmacology/therapeutic use ; Drug Resistance, Microbial ; History, 17th Century ; History, 19th Century ; History, 20th Century ; History, Ancient ; Humans ; Mycobacterium tuberculosis/drug effects ; Tuberculosis/complications/drug therapy/*epidemiology/transmission ; United States/epidemiology
    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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  • 10
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    Defining protective responses to pathogens: cytokine profiles in leprosy lesions (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-11
    Description: The immunological mechanisms required to engender resistance have been defined in few infectious diseases of man, and the role of specific cytokines is unclear. Leprosy presents clinically as a spectrum in which resistance correlates with cell-mediated immunity to the pathogen. To assess in situ cytokine patterns, messenger RNA extracted from leprosy skin biopsy specimens was amplified by the polymerase chain reaction with 14 cytokine-specific primers. In lesions of the resistant form of the disease, messenger RNAs coding for interleukin-2 and interferon-gamma were most evident. In contrast, messenger RNAs for interleukin-4, interleukin-5, and interleukin-10 predominated in the multibacillary form. Thus, resistance and susceptibility were correlated with distinct patterns of cytokine production.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamamura, M -- Uyemura, K -- Deans, R J -- Weinberg, K -- Rea, T H -- Bloom, B R -- Modlin, R L -- AI 07118/AI/NIAID NIH HHS/ -- AI 22553/AI/NIAID NIH HHS/ -- AR 40312/AR/NIAMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1991 Oct 11;254(5029):277-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Dermatology, UCLA School of Medicine 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1925582" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cytokines/genetics/*physiology ; Humans ; Immunity, Innate ; Interferon-gamma/physiology ; Interleukin-10/physiology ; Interleukin-2/physiology ; Interleukin-4/physiology ; Interleukin-5/physiology ; Leprosy/*immunology ; Molecular Sequence Data ; Polymerase Chain Reaction ; RNA, Messenger/genetics ; Skin/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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