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miR-155 and its star-form partner miR-155* cooperatively regulate type I interferon production by human plasmacytoid

Haibo Zhou1, Xinfang Huang, Huijuan Cui

  • 1Joint Molecular Rheumatology Laboratory of the Institute of Health Sciences and Shanghai Renji Hospital, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, and Shanghai Jiaotong University School of Medicine, Shanghai, China.

Blood
|September 21, 2010
PubMed

Insights

MicroRNAs regulate immune responses. This study reveals miR-155* and miR-155 have opposing roles in human plasmacytoid dendritic cell (PDC) activation by modulating type I interferon production through distinct pathways.

Area of Science:

  • Immunology
  • Molecular Biology
  • Gene Regulation

Background:

  • MicroRNAs (miRNAs) are key regulators of gene expression impacting the immune system.
  • Plasmacytoid dendritic cells (PDCs) play a crucial role in innate and adaptive immunity, particularly in type I interferon production.
  • Understanding miRNA-mediated regulation of PDC activation is vital for immune system research.

Purpose of the Study:

  • To investigate the role of specific microRNAs in the activation of human plasmacytoid dendritic cells (PDCs).
  • To elucidate the distinct mechanisms by which miR-155* and miR-155 regulate type I interferon production in PDCs.
  • To identify the regulatory networks involving miRNAs, proteins, and signaling pathways in PDC activation.

Main Methods:

  • miRNA profiling of PDCs following Toll-like receptor 7 (TLR7) stimulation.
  • Analysis of miRNA precursor processing and induction pathways (c-Jun N-terminal kinase).
  • Luciferase reporter assays to validate miRNA targets (IRAKM, TAB2) and assess effects on interferon-α/β expression.
  • Kinetic analysis of miRNA induction and investigation of posttranscriptional regulation by interferon and KHSRP.

Main Results:

  • TLR7 stimulation induced differential expression of 19 miRNAs in PDCs, with miR-155* and miR-155 being highly upregulated.
  • miR-155* augmented interferon-α/β production by suppressing IRAKM, while miR-155 inhibited it by targeting TAB2.
  • miR-155* and miR-155 exhibited distinct induction kinetics, with miR-155* peaking early and miR-155 later, suggesting cooperative roles.
  • Autocrine/paracrine type I interferon and TLR7-activated KHSRP inversely regulated miR-155* and miR-155 at the posttranscriptional level.

Conclusions:

  • miR-155* and miR-155 are critical, oppositely acting regulators of type I interferon production during PDC activation.
  • Distinct molecular targets and differential kinetic induction underlie the opposing functions of miR-155* and miR-155.
  • Novel miRNA-protein regulatory networks involving type I interferon and KHSRP are identified, providing insights into PDC activation control.

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