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  • 1
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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
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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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
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Structural requirements for glycolipid antigen recognition by CD1b-restricted T cells (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-10
    Description: The human CD1b protein presents lipid antigens to T cells, but the molecular mechanism is unknown. Identification of mycobacterial glucose monomycolate (GMM) as a CD1b-presented glycolipid allowed determination of the structural requirements for its recognition by T cells. Presentation of GMM to CD1b-restricted T cells was not affected by substantial variations in its lipid tails, but was extremely sensitive to chemical alterations in its carbohydrate or other polar substituents. These findings support the view that the recently demonstrated hydrophobic CD1 groove binds the acyl chains of lipid antigens relatively nonspecifically, thereby positioning the hydrophilic components for highly specific interactions with T cell antigen receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moody, D B -- Reinhold, B B -- Guy, M R -- Beckman, E M -- Frederique, D E -- Furlong, S T -- Ye, S -- Reinhold, V N -- Sieling, P A -- Modlin, R L -- Besra, G S -- Porcelli, S A -- AR01988/AR/NIAMS NIH HHS/ -- GM54045/GM/NIGMS NIH HHS/ -- RR10888/RR/NCRR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Oct 10;278(5336):283-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lymphocyte Biology Section, Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9323206" target="_blank"〉PubMed〈/a〉
    Keywords: *Antigen Presentation ; Antigens, Bacterial/immunology ; Antigens, CD1/chemistry/*immunology/metabolism ; Epitopes/immunology ; Glycolipids/chemistry/*immunology/metabolism ; Glycosylation ; Humans ; Ligands ; Mass Spectrometry ; Mycobacterium/immunology ; Mycolic Acids/chemistry/immunology ; Receptors, Antigen, T-Cell/immunology/metabolism ; T-Lymphocyte Subsets/*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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  • 4
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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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  • 5
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    Immunology. Now presenting: gammadelta T cells (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-07-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Modlin, Robert L -- Sieling, Peter A -- New York, N.Y. -- Science. 2005 Jul 8;309(5732):252-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Dermatology and Department of Microbiology, Immunology and Molecular Genetics, David Geffen School of Medicine, University of California-Los Angeles, 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/16002604" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigen Presentation ; Antigen-Presenting Cells/*immunology ; Dendritic Cells/immunology ; Genes, T-Cell Receptor ; Histocompatibility Antigens Class II/immunology/metabolism ; Humans ; Immunity, Active ; Immunity, Innate ; Immunologic Memory ; Lymphocyte Activation ; Mice ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; Receptors, Antigen, T-Cell, gamma-delta/*immunology ; T-Lymphocyte Subsets/*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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