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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

Mouse embryonic stem cells are deficient in type I interferon expression in response to viral infections and

Ruoxing Wang1, Jundi Wang, Amber M Paul

  • 1Department of Biological Sciences, University of Southern Mississippi, Hattiesburg, Mississippi 39406, USA.

The Journal of Biological Chemistry
|April 13, 2013
PubMed

Insights

Embryonic stem cells (ESCs) are susceptible to viral infections but cannot produce type I interferons (IFNα/β). This deficiency in innate immunity hinders their use in regenerative medicine.

Area of Science:

  • Immunology
  • Stem Cell Biology
  • Virology

Background:

  • Embryonic stem cells (ESCs) hold great promise for regenerative medicine due to their self-renewal and differentiation potential.
  • The innate immune responses of ESCs and their derivatives remain largely uncharacterized.
  • Understanding ESC immunity is crucial for their safe and effective therapeutic applications.

Purpose of the Study:

  • To investigate the innate immune responses of mouse embryonic stem cells (mESCs) to viral infections.
  • To determine the capacity of mESCs to express type I interferons (IFNα/β) upon viral challenge.
  • To elucidate the mechanisms underlying potential immune deficiencies in mESCs.

Main Methods:

  • Exposure of mESCs to live viruses (La Crosse, West Nile, Sendai) and polyinosinic:polycytidylic acid (polyIC).
  • Quantification of type I interferon (IFNα/β) expression.
  • Assessment of dsRNA-activated protein kinase (PKR) activation and cell proliferation.
  • Analysis of viral RNA receptor expression (TLR3, MDA5, RIG-I).

Main Results:

  • mESCs are susceptible to viral infection but fail to express type I interferons (IFNα/β), unlike fibroblasts.
  • PolyIC treatment, a viral dsRNA analog, induces dsRNA-activated protein kinase (PKR) in mESCs, inhibiting proliferation.
  • Key viral RNA receptors, including TLR3 and MDA5, are expressed at low levels in mESCs, and RIG-I may be inactive.

Conclusions:

  • mESCs possess functional cytosolic dsRNA-activated protein kinase (PKR) but exhibit deficient mechanisms for type I interferon (IFNα/β) expression.
  • Low expression or activity of viral RNA sensors contributes to the impaired innate immune response in mESCs.
  • These innate immune deficiencies in ESCs require consideration for their application in regenerative medicine.
Keywords:
Double-stranded RNAEmbryonic Stem CellInnate ImmunityInterferonProtein Kinase RNA (PKR)Toll-like Receptors (TLR)

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