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    Identification of a novel human MD-2 splice variant that negatively regulates Lipopolysaccharide-induced TLR4 signaling

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    Authors
    Gray, Pearl
    Michelsen, Kathrin S.
    Sirois, Cherilyn M.
    Lowe, Emily
    Shimada, Kenichi
    Crother, Timothy R.
    Chen, Shuang
    Brikos, Constantinos
    Bulut, Yonca
    Latz, Eicke
    Underhill, David
    Arditi, Moshe
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    Student Authors
    Cherilyn M. Sirois
    UMass Chan Affiliations
    Department of Medicine, Division of Infectious Diseases and Immunology
    Document Type
    Journal Article
    Publication Date
    2010-06-01
    Keywords
    Cell Line; Cell Separation; Enzyme-Linked Immunosorbent Assay; Flow Cytometry; Gene Expression; Gene Expression Profiling; Gene Expression Regulation; Humans; Immunoblotting; Immunoprecipitation; Interleukin-8; Lipopolysaccharides; Lymphocyte Antigen 96; Microscopy, Confocal; Protein Isoforms; Reverse Transcriptase Polymerase Chain Reaction; Signal Transduction; Toll-Like Receptor 4
    Immunology and Infectious Disease
    Life Sciences
    Medicine and Health Sciences
    
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    Link to Full Text
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3057206/
    Abstract
    Myeloid differentiation factor 2 (MD-2) is a secreted gp that assembles with TLR4 to form a functional signaling receptor for bacterial LPS. In this study, we have identified a novel alternatively spliced isoform of human MD-2, termed MD-2 short (MD-2s), which lacks the region encoded by exon 2 of the MD-2 gene. Similar to MD-2, MD-2s is glycosylated and secreted. MD-2s also interacted with LPS and TLR4, but failed to mediate LPS-induced NF-kappaB activation and IL-8 production. We show that MD-2s is upregulated upon IFN-gamma, IL-6, and TLR4 stimulation and negatively regulates LPS-mediated TLR4 signaling. Furthermore, MD-2s competitively inhibited binding of MD-2 to TLR4. Our study pinpoints a mechanism that may be used to regulate TLR4 activation at the onset of signaling and identifies MD-2s as a potential therapeutic candidate to treat human diseases characterized by an overly exuberant or chronic immune response to LPS.
    Source

    J Immunol. 2010 Jun 1;184(11):6359-66. Epub 2010 Apr 30.

    DOI
    10.4049/jimmunol.0903543
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/33113
    PubMed ID
    20435923
    Related Resources

    Link to article in PubMed

    ae974a485f413a2113503eed53cd6c53
    10.4049/jimmunol.0903543
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