Micro-RNA-155 inhibits IFN-γ signaling in CD4+ T cells

Authors

  • Arnob Banerjee,

    1. Abramson Family Cancer Research Institute and Department of Medicine, University of Pennsylvania, Philadelphia, PA, USA
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  • Felix Schambach,

    1. Abramson Family Cancer Research Institute and Department of Medicine, University of Pennsylvania, Philadelphia, PA, USA
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  • Caitlin S. DeJong,

    1. Abramson Family Cancer Research Institute and Department of Medicine, University of Pennsylvania, Philadelphia, PA, USA
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  • Scott M. Hammond,

    1. Department of Cell and Developmental Biology, University of North Carolina, Chapel Hill, NC, USA
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  • Steven L. Reiner

    Corresponding author
    1. Abramson Family Cancer Research Institute and Department of Medicine, University of Pennsylvania, Philadelphia, PA, USA
    • Abramson Family Cancer Research Institute, University of Pennsylvania, BRB II/III, Room 414, 421 Curie Boulevard, Philadelphia, PA 19104, USA Fax:+1-215-746-5525
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Abstract

Micro-RNA (miR) are increasingly recognized as critical regulators of tissue-specific patterns of gene expression. CD4+ T cells lacking miR-155, for example, exhibit bias towards Th2 differentiation, indicating that the absence of individual miR could alter CD4+ T-cell differentiation. We now show that miR-155 is induced upon T-cell activation and that it promotes Th1 differentiation when over-expressed in activated CD4+ T cells. Antagonism of miR-155 leads to induction of IFN-γ receptor α-chain (IFN-γRα, and a functional miR-155 target site is identified within the 3′ untranslated region of IFN-γRα. These results identify IFN-γRα as a second miR-155 target in T cells and suggest that miR-155 contributes to Th1 differentiation in CD4+ T cells by inhibiting IFN-γ signaling.

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