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  • 1
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    Differential effects of cytolytic T cell subsets on intracellular infection (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-13
    Description: In analyzing mechanisms of protection against intracellular infections, a series of human CD1-restricted T cell lines of two distinct phenotypes were derived. Both CD4(-)CD8(-) (double-negative) T cells and CD8(+) T cells efficiently lysed macrophages infected with Mycobacterium tuberculosis. The cytotoxicity of CD4(-)CD8(-) T cells was mediated by Fas-FasL interaction and had no effect on the viability of the mycobacteria. The CD8(+) T cells lysed infected macrophages by a Fas-independent, granule-dependent mechanism that resulted in killing of bacteria. These data indicate that two phenotypically distinct subsets of human cytolytic T lymphocytes use different mechanisms to kill infected cells and contribute in different ways to host defense against intracellular infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stenger, S -- Mazzaccaro, R J -- Uyemura, K -- Cho, S -- Barnes, P F -- Rosat, J P -- Sette, A -- Brenner, M B -- Porcelli, S A -- Bloom, B R -- Modlin, R L -- New York, N.Y. -- Science. 1997 Jun 13;276(5319):1684-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of California Los Angeles 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/9180075" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD1/*immunology ; Antigens, CD95/immunology/metabolism ; Cell Line ; Coculture Techniques ; Colony Count, Microbial ; Cytoplasmic Granules/immunology ; *Cytotoxicity, Immunologic ; Fas Ligand Protein ; Granzymes ; Humans ; Lymphocyte Activation ; Macrophages/*immunology/microbiology ; Membrane Glycoproteins/genetics/immunology/metabolism ; Mycobacterium tuberculosis/growth & development/*immunology ; Perforin ; Phenotype ; Pore Forming Cytotoxic Proteins ; Serine Endopeptidases/metabolism ; Strontium/pharmacology ; T-Lymphocyte Subsets/*immunology ; 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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    Use of genetic profiling in leprosy to discriminate clinical forms of the disease (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-13
    Description: Leprosy presents as a clinical and immunological spectrum of disease. With the use of gene expression profiling, we observed that a distinction in gene expression correlates with and accurately classifies the clinical form of the disease. Genes belonging to the leukocyte immunoglobulin-like receptor (LIR) family were significantly up-regulated in lesions of lepromatous patients suffering from the disseminated form of the infection. In functional studies, LIR-7 suppressed innate host defense mechanisms by shifting monocyte production from interleukin-12 toward interleukin-10 and by blocking antimicrobial activity triggered by Toll-like receptors. Gene expression profiles may be useful in defining clinical forms of disease and providing insights into the regulation of immune responses to pathogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bleharski, Joshua R -- Li, Huiying -- Meinken, Christoph -- Graeber, Thomas G -- Ochoa, Maria-Teresa -- Yamamura, Masahiro -- Burdick, Anne -- Sarno, Euzenir N -- Wagner, Manfred -- Rollinghoff, Martin -- Rea, Thomas H -- Colonna, Marco -- Stenger, Steffen -- Bloom, Barry R -- Eisenberg, David -- Modlin, Robert 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. 2003 Sep 12;301(5639):1527-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Immunology, and Molecular Genetics, David Geffen School of Medicine at University of California Los Angeles (UCLA), Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12970564" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Cluster Analysis ; Colony Count, Microbial ; Cytokines/genetics/metabolism ; *Gene Expression Profiling ; *Gene Expression Regulation ; Genes, Immunoglobulin ; Humans ; Immunity, Cellular ; Immunity, Innate ; Leprosy, Lepromatous/*classification/*genetics/immunology/physiopathology ; Leprosy, Tuberculoid/*classification/*genetics/immunology/physiopathology ; Macrophages, Alveolar/microbiology ; Membrane Glycoproteins/immunology ; Mycobacterium tuberculosis/growth & development/immunology ; Oligonucleotide Array Sequence Analysis ; Polymerase Chain Reaction ; Principal Component Analysis ; Receptors, Cell Surface/immunology ; Receptors, Immunologic/genetics/metabolism ; Toll-Like Receptors ; Up-Regulation
    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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  • 3
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    Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-25
    Description: In innate immune responses, activation of Toll-like receptors (TLRs) triggers direct antimicrobial activity against intracellular bacteria, which in murine, but not human, monocytes and macrophages is mediated principally by nitric oxide. We report here that TLR activation of human macrophages up-regulated expression of the vitamin D receptor and the vitamin D-1-hydroxylase genes, leading to induction of the antimicrobial peptide cathelicidin and killing of intracellular Mycobacterium tuberculosis. We also observed that sera from African-American individuals, known to have increased susceptibility to tuberculosis, had low 25-hydroxyvitamin D and were inefficient in supporting cathelicidin messenger RNA induction. These data support a link between TLRs and vitamin D-mediated innate immunity and suggest that differences in ability of human populations to produce vitamin D may contribute to susceptibility to microbial infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Philip T -- Stenger, Steffen -- Li, Huiying -- Wenzel, Linda -- Tan, Belinda H -- Krutzik, Stephan R -- Ochoa, Maria Teresa -- Schauber, Jurgen -- Wu, Kent -- Meinken, Christoph -- Kamen, Diane L -- Wagner, Manfred -- Bals, Robert -- Steinmeyer, Andreas -- Zugel, Ulrich -- Gallo, Richard L -- Eisenberg, David -- Hewison, Martin -- Hollis, Bruce W -- Adams, John S -- Bloom, Barry R -- Modlin, Robert L -- AI052453/AI/NIAID NIH HHS/ -- AI22553/AI/NIAID NIH HHS/ -- AI47868/AI/NIAID NIH HHS/ -- AI48176/AI/NIAID NIH HHS/ -- AR45676/AR/NIAMS NIH HHS/ -- AR50626/AR/NIAMS NIH HHS/ -- HD043921/HD/NICHD NIH HHS/ -- K22 AI085025/AI/NIAID NIH HHS/ -- RR00425/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2006 Mar 24;311(5768):1770-3. Epub 2006 Feb 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Immunology, and Molecular Genetics, University of California at Los Angeles, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16497887" target="_blank"〉PubMed〈/a〉
    Keywords: 25-Hydroxyvitamin D3 1-alpha-Hydroxylase/genetics ; African Americans ; Antimicrobial Cationic Peptides/biosynthesis/*genetics/metabolism ; Calcitriol/blood/*metabolism ; Cathelicidins ; Colony Count, Microbial ; Dendritic Cells/microbiology/physiology ; Disease Susceptibility ; Humans ; *Immunity, Innate ; Macrophages/immunology/microbiology/*physiology ; Monocytes/microbiology/*physiology ; Mycobacterium tuberculosis/*growth & development ; Oligonucleotide Array Sequence Analysis ; RNA, Messenger/genetics/metabolism ; Receptors, Calcitriol/genetics ; Steroid Hydroxylases/genetics ; Toll-Like Receptors/*physiology ; Tuberculosis/etiology/immunology ; Up-Regulation ; Vitamin D3 24-Hydroxylase
    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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