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

Eur J Immunol. 2010 Jan;40(1):225-31. doi: 10.1002/eji.200939381.

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-gamma receptor alpha-chain (IFN-gammaRalpha), and a functional miR-155 target site is identified within the 3' untranslated region of IFN-gammaRalpha. These results identify IFN-gammaRalpha 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-gamma signaling.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • CD4-Positive T-Lymphocytes / cytology
  • CD4-Positive T-Lymphocytes / immunology*
  • CD4-Positive T-Lymphocytes / metabolism
  • Cell Differentiation
  • Cells, Cultured
  • Interferon-gamma / immunology
  • Interferon-gamma / metabolism
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • MicroRNAs / genetics*
  • Receptor, Interferon alpha-beta / immunology*
  • Receptor, Interferon alpha-beta / metabolism
  • Signal Transduction*

Substances

  • MicroRNAs
  • Mirn155 microRNA, mouse
  • Receptor, Interferon alpha-beta
  • Interferon-gamma