RLR-mediated production of interferon-β by a human dendritic cell subset and its role in virus-specific immunity

J Leukoc Biol. 2012 Jul;92(1):159-69. doi: 10.1189/jlb.0711360. Epub 2012 Apr 18.

Abstract

Cytosolic RIG-I-like helicases (RLR) are PRRs involved in type I IFN production and antiviral immunity. This study focuses to the comparison of the expression, function, and signaling cascades associated to RLR in the previously identified CD14(-)DC-SIGN(+)PPARγ(low)CD1a(+) and CD14(low)DC-SIGN(+)PPARγ(high)CD1a(-) human moDC subsets. Our results revealed that the expression of RLR genes and proteins as well as the activity of the coupled signaling pathways are significantly higher in the CD1a(+) subset than in its phenotypically and functionally distinct counterpart. Specific activation of RLR in moDCs by poly(I:C) or influenza virus was shown to induce the secretion of IFN-β via IRF3, whereas induction of proinflammatory cytokine responses were predominantly controlled by TLR3. The requirement of RLR-mediated signaling in CD1a(+) moDCs for priming naïve CD8(+) T lymphocytes and inducing influenza virus-specific cellular immune responses was confirmed by RIG-I/MDA5 silencing, which abrogated these functions. Our results demonstrate the subset-specific activation of RLR and the underlying mechanisms behind its cytokine secretion profile and identify CD1a(+) moDCs as an inflammatory subset with specialized functional activities. We also provide evidence that this migratory DC subset can be detected in human tonsil and reactive LNs.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antigen-Presenting Cells / immunology
  • Antigens, CD1 / genetics
  • Antigens, CD1 / metabolism
  • Blotting, Western
  • Cell Communication
  • Cell Differentiation
  • Cells, Cultured
  • Cytokines / metabolism
  • DEAD-box RNA Helicases / genetics
  • DEAD-box RNA Helicases / metabolism*
  • Dendritic Cells / cytology
  • Dendritic Cells / immunology*
  • Dendritic Cells / virology*
  • Humans
  • Immunity, Innate*
  • Immunoenzyme Techniques
  • Influenza, Human / immunology*
  • Influenza, Human / metabolism
  • Influenza, Human / virology
  • Interferon Regulatory Factor-3 / metabolism
  • Interferon Type I / metabolism
  • Interferon-beta / metabolism*
  • Lymph Nodes / metabolism
  • Orthomyxoviridae / immunology*
  • Palatine Tonsil / metabolism
  • RNA, Messenger / genetics
  • Real-Time Polymerase Chain Reaction
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction
  • T-Lymphocytes / immunology
  • T-Lymphocytes / virology

Substances

  • Antigens, CD1
  • CD1a antigen
  • Cytokines
  • IRF3 protein, human
  • Interferon Regulatory Factor-3
  • Interferon Type I
  • RNA, Messenger
  • Interferon-beta
  • DEAD-box RNA Helicases