Anti-inflammatory properties of pro-inflammatory interferon-γ

Mühl, Heiko; Pfeilschifter, Josef

doi:10.1016/s1567-5769(03)00131-0

Cited by 238 publications

(181 citation statements)

References 117 publications

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“…IFN-␥ could modulate the level of certain proinflammatory cytokines (TNF-␣ and IL-1␣) (26). However, a regulatory role of IFN-␥ on PAR 2 expression levels is unknown.…”

Section: Stimulation With Ifn-␥ Enhances Par 2 Cell Surface Expressiomentioning

confidence: 99%

Agonists of Proteinase-Activated Receptor-2 Enhance IFN-γ-Inducible Effects on Human Monocytes: Role in Influenza A Infection

Feld¹,

Shpacovitch²,

Ehrhardt³

et al. 2008

The Journal of Immunology

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Proteinase-activated receptor-2 (PAR2) is expressed by different types of human leukocytes and involved in the development of inflammatory and infectious diseases. However, its precise role in the regulation of human monocyte and macrophage function during viral infection remains unclear. Also, the ability of PAR2 agonists to enhance the effects induced by immune mediators during infection or inflammation is still poorly investigated. Therefore, we investigated the ability of a PAR2 agonist to enhance IFN-γ-induced suppression of influenza A virus replication in human monocytes. We found that this effect correlates with an increased abundance of IκBα after costimulation of cells with PAR2 agonist and IFN-γ. Remarkably, coapplication of PAR2 agonist and IFN-γ also enhances the effects of IFN-γ on IFN-γ-inducible protein 10 kDa release, and CD64 and αVβ3 surface expression by human monocytes. Together, these findings indicate a potentially protective role of PAR2 activation during the progression of influenza A virus infection. This effect could be associated with the ability of PAR2 agonists to enhance IFN-γ-induced protective effects on human monocytes.

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“…IFN-␥ could modulate the level of certain proinflammatory cytokines (TNF-␣ and IL-1␣) (26). However, a regulatory role of IFN-␥ on PAR 2 expression levels is unknown.…”

Section: Stimulation With Ifn-␥ Enhances Par 2 Cell Surface Expressiomentioning

confidence: 99%

Agonists of Proteinase-Activated Receptor-2 Enhance IFN-γ-Inducible Effects on Human Monocytes: Role in Influenza A Infection

Feld¹,

Shpacovitch²,

Ehrhardt³

et al. 2008

The Journal of Immunology

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“…The associated IFNg production may actually be able to counteract the aforementioned tumor-promoting activities of IL-18. In fact, IFNg is able to down-regulate both IL-8 and matrix metalloprotease-9 in the human system (50,51). The beneficial effects of IL-18 may also include a correction of the antiapoptotic microenvironment characteristic for AML (52).…”

Section: Il-18 -Induced T-bet In Kg-1 Cellsmentioning

confidence: 99%

Interleukin-18 directly activates T-bet expression and function via p38 mitogen-activated protein kinase and nuclear factor-κB in acute myeloid leukemia–derived predendritic KG-1 cells

Bachmann

Drăgoi

Poleganov

et al. 2007

Molecular Cancer Therapeutics

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The leukemic cell line KG-1 was isolated from a patient with acute myeloid leukemia and is regarded a cellular model of human dendritic cell progenitors. The T helper type 1 cytokine interleukin (IL)-18 has been shown to induce the maturation of these cells towards a dendritic phenotype and, moreover, is able to mediate IFN; production in this model. Because T-box expressed in T cells (T-bet) is considered to be of paramount importance for dendritic cell function, the effects of IL-18 on this transcription factor have been investigated in the current study. Here, we show that activation of KG-1 cells by IL-18 induces T-bet mRNA and protein within 4 to 6 h of incubation. This hitherto unrecognized function of IL-18 was suppressed by the inhibition of p38 mitogen-activated protein kinase activity and nuclear factor-KB function.

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“…In contrast, we observed the levels of IFN-gamma to be lower in the patients than in the controls. In fact, IFN-gamma, in addition to acting as a local pro-inflammatory cytokine, has been shown to exert counter-inflammatory effects under specific conditions 47) . IFN-gamma levels were lower in patients with three-vessel disease than in those with one-vessel disease, indicating that the cardioprotective effect increases in association with disease severity.…”

Section: Limitationsmentioning

confidence: 99%

Expression Analysis of Leukotriene-Inflammatory Gene Interaction Network in Patients with Coronary Artery Disease

Nair¹,

Shanker²,

Jambunathan³

et al. 2014

JAT

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Aim: Leukotrienes are important lipid inflammatory mediators that play a pivotal role in the pathogenesis of atherosclerosis. We aimed to construct a network of interactions between leukotrienes and inflammatory biomarkers and evaluate the expression of key members of the leukotriene pathway and leukotriene-induced inflammatory molecules in patients with coronary artery disease (CAD) and healthy controls. Methods: Leukotrienes and their regulatory inflammatory molecules reported in the literature were used to construct a biological network employing Gene spring GX v12.5. Key leukotriene genes and their closely interacting members were selected for expression study in 64 patients and 64 matched controls. Four single nucleotide polymorphisms (SNPs) (rs6538697, rs2660898, rs17525495 and rs1978331) in the leukotriene A4 hydrolase (LTA4H) gene were genotyped using SYBR green method, and plasma leukotriene B4 (LTB4) levels were measured using ELISA. Results: The expression levels of arachidonate 5-lipoxygenase (ALOX5), LTA4H, tumor necrosis factor (TNF) and interleukin-8 (IL-8) genes were significantly higher in patients than in the controls (p＜0.05). IL-8 (r

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Anti-inflammatory properties of pro-inflammatory interferon-γ

Cited by 238 publications

References 117 publications

Agonists of Proteinase-Activated Receptor-2 Enhance IFN-γ-Inducible Effects on Human Monocytes: Role in Influenza A Infection

Agonists of Proteinase-Activated Receptor-2 Enhance IFN-γ-Inducible Effects on Human Monocytes: Role in Influenza A Infection

Interleukin-18 directly activates T-bet expression and function via p38 mitogen-activated protein kinase and nuclear factor-κB in acute myeloid leukemia–derived predendritic KG-1 cells

Expression Analysis of Leukotriene-Inflammatory Gene Interaction Network in Patients with Coronary Artery Disease

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