期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 203, 期 9, 页码 2063-2071出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20061318
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资金
- NIAID NIH HHS [AI 57831, R01 AI057831, AI 50618, R01 AI050618] Funding Source: Medline
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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