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- W2070058498 abstract "Macrophages (MØ) are used as the intracellular niche by several bacterial and protozoan microorganisms. Such microbial pathogens adopt diverse strategies to avoid MØ microbicidal effects. Recent insights into the Toxoplasma gondii-MØ interaction reveal novel ways that intracellular parasites subvert MØ function. In contrast to some microbial pathogens, Toxoplasma infection is not silent but induces rapid activation of transcription factors such as STAT-1 and NFkappaB. However, the parasite blocks nuclear translocation of both factors, and MØ cannot produce IL-12 or TNF-alpha when subsequently triggered with lipopolysaccharide. The nuclear import blockade is lifted 24 h after infection, but cells remain actively suppressed in TNF-alpha production. Nevertheless, IL-12 synthesis is initiated at this later time point. Toxoplasma gondii-induced production of this cytokine occurs through both MyD88- and CCR5-dependent pathways. The balance of cytokine subversion and stimulation during infection probably results from the parasite's need to simultaneously avoid immune elimination and trigger immunity to prevent host death." @default.
- W2070058498 created "2016-06-24" @default.
- W2070058498 creator A5011387477 @default.
- W2070058498 creator A5018306332 @default.
- W2070058498 creator A5078462457 @default.
- W2070058498 date "2003-02-01" @default.
- W2070058498 modified "2023-10-12" @default.
- W2070058498 title "In the belly of the beast: subversion of macrophage proinflammatory signalling cascades during Toxoplasma gondii infection" @default.
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- W2070058498 doi "https://doi.org/10.1046/j.1462-5822.2003.00258.x" @default.
- W2070058498 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12580944" @default.
- W2070058498 hasPublicationYear "2003" @default.
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