Orf virus IL-10 reduces monocyte, dendritic cell and mast cell recruitment to inflamed skin

Jared R Bennett1, Zabeen Lateef1, Stephen B Fleming1

  • 1Department of Microbiology and Immunology, University of Otago, Dunedin, New Zealand.

Virus Research
|January 7, 2016
PubMed

Insights

Orf virus (ORFV) produces an interleukin-10 (IL-10) homolog that impairs innate immune cell trafficking to the skin. This viral IL-10 limits monocyte, dendritic cell, and mast cell recruitment, potentially explaining ORFV

Area of Science:

  • Virology
  • Immunology
  • Dermatology

Background:

  • Orf virus (ORFV), a zoonotic parapoxvirus, causes skin disease in sheep and humans.
  • ORFV infections lead to transient inflammation and impaired innate immune cell trafficking in the skin.
  • ORFV expresses a protein homologous to interleukin-10 (IL-10), an anti-inflammatory cytokine.

Purpose of the Study:

  • To investigate the effect of ORFV-encoded IL-10 on immune cell trafficking in inflamed skin.
  • To understand how ORFV-IL-10 influences the recruitment and activation of innate immune cells.

Main Methods:

  • Utilized a murine model with lipopolysaccharide-induced skin inflammation.
  • Administered ORFV-IL-10 to assess its impact on immune cell populations.
  • Quantified immune cell recruitment (monocytes, dendritic cells, mast cells) and activation using flow cytometry.

Main Results:

  • ORFV-IL-10 significantly limited the influx of monocytes, dendritic cells, and mast cells into inflamed skin.
  • ORFV-IL-10 suppressed the activation of dendritic cells within the skin.
  • Reduced dendritic cell activation led to decreased trafficking to draining lymph nodes.

Conclusions:

  • ORFV-IL-10 plays a critical role in modulating the host immune response during infection.
  • The viral IL-10 homolog contributes to impaired innate immune cell trafficking in ORFV-infected skin.
  • This mechanism may allow ORFV to establish and maintain persistent infections by evading immune surveillance.