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    Modulators of Dendritic Cells and B cells in Lupus

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    TETDEDXLee-temple-0225E-13698.pdf
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    Genre
    Thesis/Dissertation
    Date
    2019
    Author
    Lee, Michael Hweemoon
    Advisor
    Gallucci, Stefania
    Committee member
    Caricchio, Roberto
    Monestier, Marc
    Tükel, Çagla
    Zhang, Yi
    Luning Prak, Eline T.
    Department
    Microbiology and Immunology
    Subject
    Immunology
    Autoimmunity
    B Cells
    Curli
    Dendritic Cells
    Sle
    Permanent link to this record
    http://hdl.handle.net/20.500.12613/548
    
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    DOI
    http://dx.doi.org/10.34944/dspace/530
    Abstract
    Systemic Lupus Erythematosus (SLE) is an autoimmune disease characterized by the production of autoantibodies directed against ubiquitous self-antigens, many of which are nuclear autoantigens like dsDNA and chromatin (Pisetsky, 2016), and by elevated type I interferons (IFN) (Hooks et al., 1979; Weckerle et al., 2011), a family of pro-inflammatory cytokines that have antiviral activity (Pestka et al., 2004). Microarray analysis of peripheral blood mononuclear cells (PBMC) from SLE patients discovered the increased expression of IFN-responsive genes that was named the IFN Signature (Baechler et al., 2003a; Bennett et al., 2003b; Crow et al., 2003). Genome wide association studies indicate a clear genetic component in lupus pathogenesis (Chung et al., 2011; SLEGEN et al., 2008) and murine models of SLE confirm genetic drivers of the disease (Morel, 2010; Morel et al., 2000). However, the concordance of SLE in monozygotic twins is only 30-40% (Connolly and Hakonarson, 2012), while the inc
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