• Find People
  • Campus Map
  • PiratePort
  • A-Z
    • About
    • Submit
    • Browse
    • Login
    View Item 
    •   ScholarShip Home
    • Other Campus Research
    • Open Access
    • View Item
    •   ScholarShip Home
    • Other Campus Research
    • Open Access
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    Browse

    All of The ScholarShipCommunities & CollectionsDateAuthorsTitlesSubjectsTypeDate SubmittedThis CollectionDateAuthorsTitlesSubjectsTypeDate Submitted

    My Account

    Login

    Statistics

    View Google Analytics Statistics

    Inhibition of Autoimmune Diabetes in NOD Mice by miRNA Therapy.

    Thumbnail
    View/ Open
    journal.pone.0145179.PDF (3.600Mb)

    Show full item record
    Author
    Wang, Duncheng; Shanina, Iryna; Toyofuku, Wendy M.; Horwitz, Marc S.; Scott, Mark D.
    Abstract
    Autoimmune destruction of the pancreatic islets in Type 1 diabetes is mediated by both increased proinflammatory (Teff) and decreased regulatory (Treg) T lymphocytes resulting in a significant decrease in the Treg:Teff ratio. The non-obese diabetic (NOD) mouse is an excellent in vivo model for testing potential therapeutics for attenuating the decrease in the Treg:Teff ratio and inhibiting disease pathogenesis. Here we show for the first time that a bioreactor manufactured therapeutic consisting of a complex of miRNA species (denoted as TA1) can effectively reset the NOD immune system from a proinflammatory to a tolerogenic state thus preventing or delaying autoimmune diabetes. Treatment of NOD mice with TA1 resulted in a systemic broad-spectrum upregulation of tolerogenic T cell subsets with a parallel downregulation of Teff subsets yielding a dramatic increase in the Treg:Teff ratio. Moreover, the murine-derived TA1 was highly effective in the inhibition of allorecognition of HLA-disparate human PBMC. TA1 demonstrated dose-responsiveness and exhibited equivalent or better inhibition of allorecognition driven proliferation than etanercept (a soluble TNF receptor). These findings demonstrate that miRNA-based therapeutics can effectively attenuate or arrest autoimmune disease processes and may be of significant utility in a broad range of autoimmune diseases including Type 1 diabetes.
    URI
    http://hdl.handle.net/10342/8089
    Date
    2015
    Citation:
    APA:
    Wang, Duncheng, & Shanina, Iryna, & Toyofuku, Wendy M., & Horwitz, Marc S., & Scott, Mark D.. (January 2015). Inhibition of Autoimmune Diabetes in NOD Mice by miRNA Therapy.. , (), - . Retrieved from http://hdl.handle.net/10342/8089

    Display/Hide MLA, Chicago and APA citation formats.

    MLA:
    Wang, Duncheng, and Shanina, Iryna, and Toyofuku, Wendy M., and Horwitz, Marc S., and Scott, Mark D.. "Inhibition of Autoimmune Diabetes in NOD Mice by miRNA Therapy.". . . (), January 2015. May 29, 2023. http://hdl.handle.net/10342/8089.
    Chicago:
    Wang, Duncheng and Shanina, Iryna and Toyofuku, Wendy M. and Horwitz, Marc S. and Scott, Mark D., "Inhibition of Autoimmune Diabetes in NOD Mice by miRNA Therapy.," , no. (January 2015), http://hdl.handle.net/10342/8089 (accessed May 29, 2023).
    AMA:
    Wang, Duncheng, Shanina, Iryna, Toyofuku, Wendy M., Horwitz, Marc S., Scott, Mark D.. Inhibition of Autoimmune Diabetes in NOD Mice by miRNA Therapy.. . January 2015; (): . http://hdl.handle.net/10342/8089. Accessed May 29, 2023.
    Collections
    • Open Access

    xmlui.ArtifactBrowser.ItemViewer.elsevier_entitlement

    East Carolina University has created ScholarShip, a digital archive for the scholarly output of the ECU community.

    • About
    • Contact Us
    • Send Feedback