scholarly journals Induction of nitric oxid synthase(NOS) by soluble glucocorticoid induced tumor necrosis factor receptor(sGITR) is modulated by IFN-γ in murine macrophage

2003 ◽  
Vol 35 (3) ◽  
pp. 175-180 ◽  
Author(s):  
Hyun-Hee Shin ◽  
Hyeon Woo Lee ◽  
Hye-Seon Choi
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Murine Macrophage ◽  
Nitric Oxid ◽  
Ifn Γ ◽  
Necrosis Factor

scholarly journals Recombinant glucocorticoid induced tumor necrosis factor receptor (rGITR) induces NOS in murine macrophage

FEBS Letters ◽  
2002 ◽  
Vol 514 (2-3) ◽  
pp. 275-280 ◽  
Author(s):  
Hyun-Hee Shin ◽  
Moo-Hyung Lee ◽  
Suk-Gi Kim ◽  
Yun-Hwa Lee ◽  
Byoung S Kwon ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Murine Macrophage ◽  
Necrosis Factor

scholarly journals Rapid Elimination of Toxoplasma gondii by Gamma Interferon-Primed Mouse Macrophages Is Independent of CD40 Signaling

2007 ◽  
Vol 75 (10) ◽  
pp. 4799-4803 ◽  
Author(s):  
Yanlin Zhao ◽  
Douglas Wilson ◽  
Suzanne Matthews ◽  
George S. Yap
Keyword(s):  
Toxoplasma Gondii ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Receptor Gene ◽  
Tumor Necrosis Factor Receptor ◽  
Gamma Interferon ◽  
Primary Role ◽  
Cd40 Ligation ◽  
Ifn Γ ◽  
Necrosis Factor

ABSTRACT Autophagy has been implicated in the intracellular destruction of Toxoplasma gondii by primed macrophages following gamma interferon (IFN-γ) activation of p47 GTPases. CD40 ligation has also been shown to trigger autophagic elimination of T. gondii independent of IFN-γ and p47 GTPases. Here we demonstrate that IFN-γ/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-γ receptor gene neither clear the parasites nor repress their proliferation. Thus, CD40 and IFN-γ-induced pathogen elimination might represent two independent resistance pathways, the latter of which plays a primary role in anti-Toxoplasma immunity in mice.

scholarly journals Trypanosoma cruzi Infection in Tumor Necrosis Factor Receptor p55-Deficient Mice

1998 ◽  
Vol 66 (6) ◽  
pp. 2960-2968 ◽  
Author(s):  
Esmeralda Castaños-Velez ◽  
Stephanie Maerlan ◽  
Lyda M. Osorio ◽  
Frederik Åberg ◽  
Peter Biberfeld ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Tumor Necrosis Factor ◽  
Trypanosoma Cruzi ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Lymphoid Tissues ◽  
B Cell Differentiation ◽  
Ifn Γ ◽  
Necrosis Factor

ABSTRACT Tumor necrosis factor receptor p55 (TNFRp55) mediates host resistance to several pathogens by allowing microbicidal activities of phagocytes. In the studies reported here, TNFRp55−/− mice infected with the intracellular parasite Trypanosoma cruzishowed clearly higher parasitemia and cumulative mortality than wild-type (WT) controls did. However, gamma interferon (IFN-γ)-activated macrophages from TNFRp55−/− mice produced control levels of nitric oxide and killed the parasite efficiently in vitro. Trypanocidal mechanisms of nonphagocytic cells (myocardial fibroblasts) from both TNFRp55−/− and WT mice were also activated by IFN-γ in a dose-dependent way. However, IFN-γ-activated TNFRp55−/− nonphagocytes showed less effective killing of T. cruzi than WT control nonphagocytes, even when interleukin 1β (IL-1β) was added as a costimulator. In vivo, T. cruzi-infected TNFRp55−/− mice and WT mice released similar levels of NO and showed similar levels of IFN-γ mRNA and inducible nitric oxide synthase mRNA in their tissues. Instead, increased susceptibility toT. cruzi of TNFRp55−/− mice was associated with reduced levels of parasite-specific immunoglobulin G (IgG) (but not IgM) antibodies during infection, which is probably linked to abnormal B-cell differentiation in secondary lymphoid tissues of the mutant mice. Surprisingly, T. cruzi-infected TNFRp55−/− mice showed increased inflammatory and necrotic lesions in several tissues, especially in skeletal muscles, indicating that TNFRp55 plays an important role in controlling the inflammatory process. Accordingly, levels of Mn2+superoxide dismutase mRNA, a TNF-induced enzyme which protects the cell from the toxic effects of superoxide, were lower in mutant than in WT infected mice.

scholarly journals Increased Mortality and Dysregulated Cytokine Production in Tumor Necrosis Factor Receptor 1-Deficient Mice following Systemic Klebsiella pneumoniae Infection

2003 ◽  
Vol 71 (9) ◽  
pp. 4891-4900 ◽  
Author(s):  
Thomas A. Moore ◽  
Michelle L. Perry ◽  
Andrew G. Getsoian ◽  
Christine L. Monteleon ◽  
Anna L. Cogen ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Klebsiella Pneumoniae ◽  
Tumor Necrosis ◽  
Cytokine Production ◽  
Lymphocyte Subsets ◽  
Tumor Necrosis Factor Receptor ◽  
Tnf Α ◽  
Ifn Γ ◽  
Deficient Mice ◽  
Necrosis Factor

ABSTRACT A significant clinical complication of pulmonary infections with Klebsiella pneumoniae is peripheral blood dissemination, resulting in a systemic infection concurrent with the localized pulmonary infection. In this context, little is known about the role of tumor necrosis factor receptor 1 (TNFR1)-mediated innate immune responses during systemic Klebsiella infections. Mice lacking TNFR1 were significantly more susceptible to Klebsiella-induced mortality following intravenous inoculation. Bacterial clearance was impaired in TNFR1-deficient mice at early times following infection. Unexpectedly, bacterial burdens at the onset of mortality (days 2 to 3 postinfection) were not higher in mice lacking TNFR1. However, elevated production of liver-associated proinflammatory cytokines (interleukin-12, tumor necrosis factor alpha [TNF-α[, and gamma interferon [IFN-γ]) and chemokines (MIP-1α, MIP-2, and MCP-1) was observed within the first 24 h of infection. Additionally, excessive plasma-associated IFN-γ was also observed late in the course of infection (day 3). Spleen cells from day-3 infected TNFR1-deficient mice secreted markedly enhanced levels of IFN-γ when cultured in vitro. Additionally, there was a marked increase in the total number of activated lymphocyte subsets as indicated by CD69 upregulation. A notable exception was the sharp decrease in the frequency of splenic NK T cells in infected TNFR1 knockout (KO) mice. Anti-TNF-α therapy in TNFR1 KO mice significantly reduced chemokine production and liver injury. Combined, these data indicate a dysregulated antibacterial host response following intravenous Klebsiella infection in the absence of TNFR1 signaling, resulting in heightened cytokine production and hyperactivation of specific splenic lymphocyte subsets.

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