Migration and maturation of human dendritic cells infected with Toxoplasma gondii depend on parasite strain type

Julien Diana1, Florence Persat, Marie-Jeanne Staquet

  • 1EA3732, Université Claude Bernard LYON I, Pavillon R, Hôpital Edouard Herriot, 5 place d'Arsonval, 69437 Lyon 03, France.

Insights

Toxoplasma gondii strains differentially affect human dendritic cell (DC) functions. Low virulent strains promote DC migration via soluble factors, while virulent strains trigger DC maturation, with type II strains inhibiting this process.

Area of Science:

  • Immunology
  • Cell Biology
  • Parasitology

Background:

  • Dendritic cells (DCs) are crucial immune regulators.
  • Toxoplasma gondii (T. gondii) is an opportunistic parasite impacting host immunity.
  • Understanding parasite-host interactions at the cellular level is vital.

Purpose of the Study:

  • To investigate the effects of different T. gondii strains on human CD34+ progenitor-derived dendritic cell (DC) migration and maturation.
  • To identify parasite-derived factors influencing DC behavior.

Main Methods:

  • In vitro model using human CD34+ progenitor cells.
  • Infection with virulent (Type I) and low virulent (Type II) T. gondii strains.
  • Assessment of DC migration towards MIP-3beta.
  • Analysis of DC maturation markers.
  • Investigation of soluble factors secreted by T. gondii.

Main Results:

  • Both Type I and Type II T. gondii strains induced DC migration towards MIP-3beta.
  • Type II strains elicited a significantly higher percentage of migrating DCs compared to Type I strains or controls.
  • Virulent strains triggered DC maturation, whereas Type II strains and heat-killed tachyzoites did not.
  • A soluble factor from Type II strains inhibited DC maturation.

Conclusions:

  • T. gondii strain type dictates its impact on DC migration and maturation.
  • Parasite-secreted soluble factors play a significant role in modulating DC functions.
  • These findings highlight T. gondii's sophisticated manipulation of host immune cells.