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Enveloped viruses disable innate immune responses in dendritic cells by direct activation of TAM receptors

Suchita Bhattacharyya1, Anna Zagórska, Erin D Lew

  • 1Nomis Center for Immunobiology and Microbial Pathogenesis, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.

Cell Host & Microbe
|August 20, 2013
PubMed

Insights

Viruses engage Tyro3/Axl/Mer (TAM) receptors by binding Gas6 and Protein S to suppress immune signaling. This viral mechanism allows for immune evasion and promotes infection, highlighting TAM receptors as therapeutic targets.

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Tyro3/Axl/Mer (TAM) receptor tyrosine kinases regulate immune responses and apoptotic cell clearance.
  • Enveloped viruses utilize phosphatidylserine on their membranes to interact with Gas6 and Protein S, ligands for TAM receptors.

Purpose of the Study:

  • To investigate the role of TAM receptors in viral immune evasion.
  • To determine if viruses exploit TAM receptors to dampen host antiviral responses.

Main Methods:

  • Activation of TAM receptors on dendritic cells (DCs) using ligand-coated viruses.
  • Analysis of type I interferon (IFN) signaling in wild-type and TAM-deficient DCs.
  • Assessment of viral infection resistance in DCs with altered TAM receptor activity.
  • Use of neutralizing type I IFN antibodies and a TAM kinase inhibitor.

Main Results:

  • Ligand-coated viruses activate TAM receptors on DCs, leading to suppressed type I IFN signaling.
  • TAM-deficient DCs exhibit elevated type I IFN responses and are more resistant to viral infection.
  • Restoration of infection in TAM-deficient DCs is possible with type I IFN neutralization.
  • Inhibition of TAM kinase activity reduces viral infection in wild-type DCs.

Conclusions:

  • Viruses engage TAM receptors to attenuate type I IFN signaling, facilitating immune evasion and infection.
  • TAM receptors represent a potential therapeutic target for antiviral strategies.

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