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Cell Rep. 2014 Jun 12;7(5):1716-1728. doi: 10.1016/j.celrep.2014.04.031. Epub 2014 May 22.

Impact of regulated secretion on antiparasitic CD8 T cell responses.

Author information

1
Division of Immunology and Pathogenesis, Department of Molecular and Cellular Biology, University of California, Berkeley, Berkeley, CA 94720-3200, USA.
2
Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305-5124, USA.
3
Center of Pathophysiology of Toulouse-Purpan, INSERM UMR1043-CNRS UMR5282, University of Toulouse, 31024 Toulouse Cedex 3, France.
4
Division of Immunology and Pathogenesis, Department of Molecular and Cellular Biology, University of California, Berkeley, Berkeley, CA 94720-3200, USA. Electronic address: nshastri@berkeley.edu.
5
Division of Immunology and Pathogenesis, Department of Molecular and Cellular Biology, University of California, Berkeley, Berkeley, CA 94720-3200, USA. Electronic address: erobey@berkeley.edu.

Abstract

CD8 T cells play a key role in defense against the intracellular parasite Toxoplasma, but why certain CD8 responses are more potent than others is not well understood. Here, we describe a parasite antigen, ROP5, that elicits a CD8 T cell response in genetically susceptible mice. ROP5 is secreted via parasite organelles termed rhoptries that are injected directly into host cells during invasion, whereas the protective, dense-granule antigen GRA6 is constitutively secreted into the parasitophorous vacuole. Transgenic parasites in which the ROP5 antigenic epitope was targeted for secretion through dense granules led to enhanced CD8 T cell responses, whereas targeting the GRA6 epitope to rhoptries led to reduced CD8 responses. CD8 T cell responses to the dense-granule-targeted ROP5 epitope resulted in reduced parasite load in the brain. These data suggest that the mode of secretion affects the efficacy of parasite-specific CD8 T cell responses.

PMID:
24857659
PMCID:
PMC4057976
DOI:
10.1016/j.celrep.2014.04.031
[Indexed for MEDLINE]
Free PMC Article

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