Interleukin 12 and tumor necrosis factor alpha are costimulators of interferon gamma production by natural killer cells in severe combined immunodeficiency mice with listeriosis, and interleukin 10 is a physiologic antagonist.

Tripp, Catherine S.; Wolf, Stanley F.; Unanue, Emil R.

doi:10.1073/pnas.90.8.3725

Cited by 710 publications

(521 citation statements)

References 25 publications

(8 reference statements)

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“…Previous studies have also suggested that TNF- § in combination with or without IFN-+ plays an important role in activating resident macrophages to kill intracellular pathogens such as L. monocytogenes and T. gondii [4, [38][39][40][41][42]. However, no correlation was observed between the increase of resistance and in vitro TNF- § production in this study (Fig.…”

Section: Discussioncontrasting

confidence: 58%

“…5D, left panel). Besides IFN-+ , other cytokines such as TNF- § have also been proposed to be an important factor in resistance to intracellular pathogens [4, [38][39][40][41][42]. However, in contrast to IFN-+ , substantial levels of TNF- § were produced by + c -/-(y) -Rag-2 -/-splenocytes with or without exogenous APC fractions in response to L. monocytogenes, and no apparent correlation was observed between the amounts of TNF- § and the susceptibility to L. monocytogenes (Fig.…”

Section: Adoptive Transfer Of Ifn-q -Producing Apc Provides Resistancmentioning

confidence: 99%

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In vivo role of IFN‐γ produced by antigen‐presenting cells in early host defense against intracellular pathogens

et al. 2003

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Antigen-presenting cells (APC), including dendritic cells and macrophages, produce a large amount of interferon (IFN)-+ , a crucial cytokine for the control of infectious diseases. To elucidate the role of IFN-+ from APC in vivo, we employed cytokine receptor common + subunit ( + c) and recombination-activating gene (Rag)-2 double-knockout ( + c -/-(y) -Rag-2 -/-) mice, which are severely impaired in IFN-+ production and are extremely susceptible to infection of intracellular pathogens including Listeria monocytogenes and Toxoplasma gondii. Adoptive transfer of IFN-+ -producing APC increased levels of serum IFN-+ and the resistance to Listeria. Although depletion of NK cells from Rag-2 -/-mice slightly increased the susceptibility to bacterial infection, they are substantially more resistant than + c -/-(y) -Rag-2 -/-mice, which are also devoid of all lymphoid cells. These results demonstrate that the APC-derived IFN-+ contributes to the control of infectious agents in vivo.

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Section: Discussioncontrasting

confidence: 58%

Section: Adoptive Transfer Of Ifn-q -Producing Apc Provides Resistancmentioning

confidence: 99%

In vivo role of IFN‐γ produced by antigen‐presenting cells in early host defense against intracellular pathogens

et al. 2003

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“…It is secreted by a variety of cells including T helper cells, monocytes, macrophages, B cells, and keratinocytes (Moore et al 1993). In vitro studies demonstrate that IL-10 limits production of cytokines such as IL-1, IL-6, TNF-α, granulocyte-macrophage colony-stimulating factor, and IL-12, the generation of reactive oxygen intermediates, and the expression of surface MHC class II and co-stimulatory molecules (Tripp et al 1993;Fiorentino et al 1991;D'Andrea et al 1993). Furthermore, IL-10 directly inhibits IFN-γ production and activity in the innate and adaptive immune system via its action on NK and T cells (Chomarat et al 1993;Moore et al 1993).…”

Section: Discussionmentioning

confidence: 99%

Inflammation and mortality in a frail mouse model

Qin

et al. 2011

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Mice homozygous for targeted deletion of the interleukin 10 gene (Il-10) have been partially characterized as a model for human frailty. These mice have increased serum interleukin (IL)-6 in midlife, skeletal muscle weakness, and an altered skeletal muscle gene expression profile compared to age and sex-matched C57BL/6 (B6) control mice. In order to further characterize for use as a frailty model, we evaluated the evolution of inflammatory pathway activation, endocrine change, and mortality in these mice. Serum was collected in groups of ageand sex-matched B6.129P2-Il10 tm1Cgn /J (IL-10 tm/tm ) mice and B6 control mice at age 12, 24, 48, 72, and 90 weeks. Cytokines including IL-6, interleukin 1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ), chemokine (C-X-C motif) ligand 1 (KC), IL-12, and IL-10 were measured using electro-chemiluminescent multiplex immunoassay and insulin-like growth factor 1 (IGF-1) was measured using solid-phase enzyme-linked immunosorbent assay. A separate longitudinal cohort was monitored from age 35 weeks to approximately 100 weeks. Survival was evaluated by Kaplan-Meier survival estimates and detailed necropsy information was gathered in a subset of mice that died or were sacrificed. In IL-10 tm/tm mice compared to B6 controls, serum IL-6, IL-1β, TNF-α, IFN-γ, KC levels were significantly elevated across the age groups, serum mean IGF-1 levels were higher in the 48-week-old groups, and overall mortality rate was significantly higher. The quadratic relationship between IGF-1 and age was significantly different between the two strains of mice. Serum IL-6 was positively associated with IGF-1 but the effect was significantly larger in IL-10 tm/tm mice. These findings provide additional rationale for the use of the IL-10 tm/tm mouse as a model for frailty and for lowgrade inflammatory pathway activation.

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“…4 We have focused on TNF-␣ as a proinflammatory cytokine in the following experiments because it is secreted by macrophages after the phagocytosis of parasites and IFN-␥ is secondarily secreted by NK cells following stimulation of IL-12 and TNF-␣. 32 No TNF-␣ was observed in any organs or the serum of untreated mice (data not shown). Much higher amounts of TNF-␣ were observed in the liver and spleen of saline-pretreated mice after i.v.…”

Section: Increases In the Liver And Spleen After Lipoplex Injection Amentioning

confidence: 91%

The role of tissue macrophages in the induction of proinflammatory cytokine production following intravenous injection of lipoplexes

et al. 2002

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Recent studies have demonstrated that intravenous administration of a plasmid DNA-cationic liposome complex (lipoplex) induced significant proinflammatory cytokine production in blood and inhibited transgene expression in pulmonary endothelial cells. In this study, we examined the effects of gadolinium chloride (GdCl 3 ) pretreatment on the biodistribution and induction of proinflammatory cytokine production and transgene expression after intravenous injection of a lipoplex in mice. GdCl 3 is known to transiently deplete liver Kupffer cells and spleen macrophages after intravenous administration. Intravenous administration of a lipoplex triggers high levels of proinflammatory cytokine production, such as TNF-␣, IFN-␥ and IL-12 in serum and

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Interleukin 12 and tumor necrosis factor alpha are costimulators of interferon gamma production by natural killer cells in severe combined immunodeficiency mice with listeriosis, and interleukin 10 is a physiologic antagonist.

Cited by 710 publications

References 25 publications

In vivo role of IFN‐γ produced by antigen‐presenting cells in early host defense against intracellular pathogens

In vivo role of IFN‐γ produced by antigen‐presenting cells in early host defense against intracellular pathogens

Inflammation and mortality in a frail mouse model

The role of tissue macrophages in the induction of proinflammatory cytokine production following intravenous injection of lipoplexes

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