Abstract
Toll-like receptor 4 (TLR4) mediates lipopolysaccharide (LPS) signaling in a variety of cell types. MD-2 is associated with the extracellular domain of TLR4 and augments TLR4-dependent LPS responses in vitro. Moreover, mice lacking MD-2 (MD-2(-/-)) do not respond to LPS, survive endotoxin shock, and are susceptible to Salmonella typhimurium infection. Here, we further show that B cells lacking MD-2 do not up-regulate CD23 in response to LPS. TLR4 predominantly resides in the Golgi apparatus without MD-2. MD-2 is essential for LPS responses in vivo.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antigens, Surface / pharmacology*
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B-Lymphocytes / immunology*
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Cell Culture Techniques
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Fibroblasts
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Golgi Apparatus
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Humans
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Lipopolysaccharides / pharmacology*
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Lymphocyte Antigen 96
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Membrane Glycoproteins / genetics
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Membrane Glycoproteins / pharmacology*
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Mice
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Receptors, Cell Surface / genetics
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Receptors, IgE / biosynthesis
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Salmonella Infections, Animal
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Salmonella typhimurium / pathogenicity
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Signal Transduction
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Toll-Like Receptor 4
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Toll-Like Receptors
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Up-Regulation
Substances
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Antigens, Surface
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LY96 protein, human
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Lipopolysaccharides
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Lymphocyte Antigen 96
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Membrane Glycoproteins
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Receptors, Cell Surface
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Receptors, IgE
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TLR4 protein, human
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Toll-Like Receptor 4
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Toll-Like Receptors