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

Arnob Banerjee1, Felix Schambach, Caitlin S DeJong

  • 1Abramson Family Cancer Research Institute and Department of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

European Journal of Immunology
|October 31, 2009
PubMed

Insights

Micro-RNA 155 (miR-155) promotes Th1 cell differentiation by inhibiting interferon-gamma signaling. Its antagonism leads to increased IFN-gamma receptor alpha-chain expression in CD4+ T cells.

Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • Micro-RNAs (miRs) are key regulators of gene expression.
  • Absence of miR-155 in CD4+ T cells leads to Th2 differentiation bias.
  • miR-155's role in T-cell differentiation requires further elucidation.

Purpose of the Study:

  • To investigate the role of miR-155 in CD4+ T-cell differentiation.
  • To identify downstream targets of miR-155 in T cells.

Main Methods:

  • T-cell activation and differentiation assays.
  • Over-expression and antagonism of miR-155.
  • Identification of miR-155 target sites using bioinformatics and luciferase assays.
  • Analysis of IFN-gamma receptor alpha-chain (IFN-gammaRalpha) expression.

Main Results:

  • miR-155 is induced upon T-cell activation.
  • Over-expression of miR-155 promotes Th1 differentiation.
  • Antagonism of miR-155 upregulates IFN-gammaRalpha.
  • A functional miR-155 target site was identified in the 3' UTR of IFN-gammaRalpha.

Conclusions:

  • miR-155 promotes Th1 differentiation in CD4+ T cells.
  • IFN-gammaRalpha is a direct miR-155 target in T cells.
  • miR-155 regulates Th1 differentiation by modulating IFN-gamma signaling.

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