Inhibition of dendritic cell maturation by herpes simplex virus

Eur J Immunol. 1999 Oct;29(10):3245-53. doi: 10.1002/(SICI)1521-4141(199910)29:10<3245::AID-IMMU3245>3.0.CO;2-X.

Abstract

Maturation of dendritic cells (DC), leading to migration and increased T cell stimulatory capacity, is essential for the initiation of immune responses. This process is triggered by a variety of stimuli, such as inflammatory cytokines, bacterial and viral products. Using a recombinant disabled infectious single cycle herpes simplex virus 1 (HSV-1) encoding green fluorescent protein, we show that the infected DC are defective in up-regulating co-stimulatory molecules, do not produce cytokines, and do not acquire responsiveness to chemokines required for migration to secondary lymphoid organs. These results reveal yet another strategy used by HSV-1 to evade the immune response, namely the inhibition of signaling pathways involved in DC maturation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Adhesion Molecules
  • Cell Differentiation / immunology
  • Cells, Cultured
  • Dendritic Cells / immunology*
  • Dendritic Cells / virology
  • Herpesvirus 1, Human / immunology*
  • Herpesvirus 1, Human / pathogenicity
  • Humans
  • Interleukin-10 / biosynthesis
  • Interleukin-6 / biosynthesis
  • Lymphocyte Activation
  • Membrane Glycoproteins / biosynthesis
  • Nectins
  • Receptors, Tumor Necrosis Factor*
  • Receptors, Tumor Necrosis Factor, Member 14
  • Receptors, Virus / biosynthesis
  • T-Lymphocytes / immunology
  • Tumor Necrosis Factor-alpha / biosynthesis

Substances

  • Cell Adhesion Molecules
  • Interleukin-6
  • Membrane Glycoproteins
  • Nectins
  • Receptors, Tumor Necrosis Factor
  • Receptors, Tumor Necrosis Factor, Member 14
  • Receptors, Virus
  • TNFRSF14 protein, human
  • Tumor Necrosis Factor-alpha
  • Interleukin-10