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Dendritic cell responses during acute infection with different strains of Toxoplasma gondii determine CD8+ T cell responses and parasite burden
Author(s) -
Tait Elia Dion,
Wilson Emma,
Harris Tajie,
Jordan Kim,
Pew Marion Pepper,
Dzierszinski Florence,
Roos David,
Hunter Christopher A.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.504
Subject(s) - biology , toxoplasma gondii , virology , cd8 , immune system , intracellular parasite , cytotoxic t cell , antigen , microbiology and biotechnology , t cell , immunity , immunology , antibody , in vitro , biochemistry
The intracellular protozoan parasite Toxoplasma gondii infects a wide range of mammalian hosts. Multiple strains, defined by genotype and virulence, exist in the natural pool of T. gondii isolates. Type I strains are lethal in the mouse model, while type II strains establish chronic infections. Protective immunity to all strains is cell‐mediated; however, there are marked differences in the immune response against a type I strain versus a type II strain. Transgenic parasites that express ovalbumin (OVA) were used to examine the phenotype of antigen‐specific CD8+ T cells and dendritic cells (DC) from mice infected with RH, a type I strain, or Prugniuad (Pru), a type II strain. Mice infected with RH failed to generate as many OVA‐specific CD8+ T cells as mice infected with Pru. RH‐infected mice also had fewer DC at the site of infection in the peritoneal cavity. Using mice expressing the simian diphtheria toxin receptor under the CD11c promoter, DC were depleted 24 hours prior to Pru infection to investigate the role of DC in the generation of CD8+ T cell responses. Pru‐infected, DC‐depleted mice failed to generate antigen‐specific CD8+ T cells, produced low levels of interferon‐γ, and had increased parasite burdens. These data are consistent with a model of immunity to T. gondii in which strain‐dependent DC responses shape the generation of antigen‐specific CD8+ T cells and determine parasite burden.