Death receptor ligation or exposure to perforin trigger rapid egress of the intracellular parasite Toxoplasma gondii

J Immunol. 2007 Dec 15;179(12):8357-65. doi: 10.4049/jimmunol.179.12.8357.

Abstract

The obligate intracellular parasite Toxoplasma gondii chronically infects up to one-third of the global population, can result in severe disease in immunocompromised individuals, and can be teratogenic. In this study, we demonstrate that death receptor ligation in T. gondii-infected cells leads to rapid egress of infectious parasites and lytic necrosis of the host cell, an active process mediated through the release of intracellular calcium as a consequence of caspase activation early in the apoptotic cascade. Upon acting on infected cells via death receptor- or perforin-dependent pathways, T cells induce rapid egress of infectious parasites able to infect surrounding cells, including the Ag-specific effector cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis
  • Calcium / metabolism
  • Caspases / metabolism
  • Cell Line
  • Cytotoxicity, Immunologic*
  • Humans
  • Mice
  • Mice, Congenic
  • Perforin / genetics
  • Perforin / metabolism*
  • Receptors, Death Domain / metabolism*
  • T-Lymphocytes, Cytotoxic / immunology*
  • T-Lymphocytes, Cytotoxic / parasitology
  • Toxoplasma / immunology*
  • fas Receptor / metabolism

Substances

  • Receptors, Death Domain
  • fas Receptor
  • Perforin
  • Caspases
  • Calcium