The Journal of Experimental Medicine
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Published online 28 August 2006 doi:10.1084/jem.20061318
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 9, 2063-2071
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BRIEF DEFINITIVE REPORT

 Vacuolar and plasma membrane stripping and autophagic elimination of Toxoplasma gondii in primed effector macrophages

Yun M. Ling1, Michael H. Shaw1, Carol Ayala2, Isabelle Coppens3, Gregory A. Taylor4, David J.P. Ferguson5, and George S. Yap1

1 Department of Molecular Microbiology and Immunology, Division of Biology and Medicine, Brown University, Providence, RI 02912
2 Core Research Laboratories, Rhode Island Hospital, Providence, RI 02903
3 Department of Molecular Microbiology and Immunology, Johns Hopkins University School of Public Health, Baltimore, MD 21205
4 Department of Medicine, Department of Molecular Genetics & Microbiology, Department of Immunology, and Center for the Study of Aging, Duke University and GRECC VA Medical Center, Durham, NC 27710
5 Nuffield Department of Pathology, John Radcliffe Hospital, Oxford University, Oxford OX3 9DU, UK

CORRESPONDENCE George S. Yap: George_Yap{at}brown.edu

Apicomplexan protozoan pathogens avoid destruction and establish a replicative niche within host cells by forming a nonfusogenic parasitophorous vacuole (PV). Here we present evidence for lysosome-mediated degradation of Toxoplasma gondii after invasion of macrophages activated in vivo. Pathogen elimination was dependent on the interferon {gamma} inducible-p47 GTPase, IGTP, required PI3K activity, and was preceded by PV membrane indentation, vesiculation, disruption, and, surprisingly, stripping of the parasite plasma membrane. Denuded parasites were enveloped in autophagosome-like vacuoles, which ultimately fused with lysosomes. These observations outline a series of mechanisms used by effector cells to redirect the fate of a classically nonfusogenic intracellular pathogen toward a path of immune elimination.


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