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Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
08:32

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production

Published on: March 2, 2014

Matrix protein mediated shutdown of host cell metabolism limits vesicular stomatitis virus-induced interferon-alpha

Zoe Waibler1, Claudia N Detje, John C Bell

  • 1Division of Immunology, Paul-Ehrlich-Institut, D-63225, Langen, Germany. waizo@pei.de

Immunobiology
|December 19, 2007
PubMed

Insights

Plasmacytoid dendritic cells (pDCs) and myeloid dendritic cells (mDCs) respond differently to viral infections. Complex virus-host interactions, not just receptor presence, dictate type I interferon production by dendritic cells.

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Plasmacytoid dendritic cells (pDCs) are known for producing type I interferons (IFN-alpha/beta) upon viral infection.
  • Conventional myeloid dendritic cells (mDCs) typically exhibit a different response profile compared to pDCs during viral encounters.

Purpose of the Study:

  • Investigate the differential induction of IFN-alpha production between pDCs and mDCs upon vesicular stomatitis virus (VSV) infection.
  • Elucidate the underlying mechanisms governing these distinct responses in dendritic cell subsets.

Main Methods:

  • Differentiated pDCs and mDCs from bone marrow cells (BM-DC).
  • Infected BM-pDC and BM-mDC with VSV and a mutant VSV (VSV-M2).
  • Assessed IFN-alpha production, RNA levels of RIG-I and TLR7, and nuclear export factors (Nup96/98).

Main Results:

  • BM-pDC produced IFN-alpha upon VSV infection, while BM-mDC did not.
  • Both DC subsets produced significant IFN-alpha upon infection with VSV-M2.
  • IFN-alpha production in response to VSV-M2 was dependent on viral replication; both subsets had comparable RIG-I and TLR7 RNA levels.
  • BM-pDC, but not BM-mDC, upregulated Nup96/98 mRNA levels upon virus infection.

Conclusions:

  • Dendritic cell type I interferon production is not solely determined by cellular receptor configurations.
  • Complex virus-host cell interactions play a crucial role in dictating IFN-alpha responses.
  • Differential expression of nuclear export factors may represent a mechanism for immune evasion or response modulation.

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