Rapid Elimination of Toxoplasma Gondii by Gamma Interferon-primed Mouse Macrophages is Independent of Cd40 Signaling.
From: Department of Molecular Microbiology and Immunology, Warren Alpert Medical School, Brown University, Providence, RI 02912, USA.
Infection and immunity
- Publish Date: Oct 2007
- ISSN: 0019-9567
- Volume: 75
- Issue: 10
- Pages: 4799-803
- Medium: Print
- Language: English
- Citation (JAMA): Zhao Yanlin, Wilson Douglas, Matthews Suzanne, et al. Rapid Elimination of Toxoplasma Gondii by Gamma Interferon-primed Mouse Macrophages is Independent of Cd40 Signaling.. Infect. Immun. Oct 2007;75:4799-803
Abstract
Autophagy has been implicated in the intracellular destruction of Toxoplasma gondii by primed macrophages following gamma interferon (IFN-gamma) activation of p47 GTPases. CD40 ligation has also been shown to trigger autophagic elimination of T. gondii independent of IFN-gamma and p47 GTPases. Here we demonstrate that IFN-gamma/p47 GTPase-dependent elimination of T. gondii by strain CPS vaccine-primed macrophages is independent of CD40/tumor necrosis factor signaling. Similar to wild-type controls, both CD40-deficient and tumor necrosis factor receptor 1/2 (TNFR1/2)-deficient macrophages can efficiently eliminate invaded strain GFP-PTG and restrain its replication following priming. In contrast, macrophages from mice lacking the IFN-gamma receptor gene neither clear the parasites nor repress their proliferation. Thus, CD40 and IFN-gamma-induced pathogen elimination might represent two independent resistance pathways, the latter of which plays a primary role in anti-Toxoplasma immunity in mice.
Mesh Headings (Keywords): Animals, Antigens, CD40, Cells, Cultured, Female, Interferon Type II, Macrophages, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Receptors, Tumor Necrosis Factor, Type I, Receptors, Tumor Necrosis Factor, Type II, Signal Transduction, Toxoplasma
Check for Full Text / PubMed Unique Identifier (PMID): 17682046
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