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  • 1
    Publication Date: 2004-08-25
    Description: Microbial products are sensed through Toll-like receptors (TLRs) and trigger a program of dendritic cell (DC) maturation that enables DCs to activate T cells. Although an accepted hallmark of this response is eventual down-regulation of DC endocytic capacity, we show that TLR ligands first acutely stimulate antigen macropinocytosis, leading to enhanced presentation on class I and class II major histocompatibility complex molecules. Simultaneously, actin-rich podosomes disappear, which suggests a coordinated redeployment of actin to fuel endocytosis. These reciprocal changes are transient and require p38 and extracellular signal-regulated kinase activation. Thus, the DC actin cytoskeleton can be rapidly mobilized in response to innate immune stimuli to enhance antigen capture and presentation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉West, Michele A -- Wallin, Robert P A -- Matthews, Stephen P -- Svensson, Henrik G -- Zaru, Rossana -- Ljunggren, Hans-Gustaf -- Prescott, Alan R -- Watts, Colin -- G0100536/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2004 Aug 20;305(5687):1153-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cell Biology and Immunology, Wellcome Trust Biocentre, School of Life Sciences, University of Dundee, Dundee DD1 5EH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15326355" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*physiology ; Animals ; Antigen Presentation ; Antigens/*immunology ; Cell Membrane/physiology/ultrastructure ; Cells, Cultured ; Cytoskeleton/*physiology/ultrastructure ; Dendritic Cells/*immunology ; Down-Regulation ; Endocytosis ; Ligands ; Lipopolysaccharides/immunology ; Membrane Glycoproteins/*metabolism ; Mice ; Microscopy, Fluorescence ; Microscopy, Video ; Mitogen-Activated Protein Kinases/metabolism ; Pinocytosis ; Receptors, Cell Surface/*metabolism ; Signal Transduction ; Toll-Like Receptors
    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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