Cytokine regulation of human monocyte interleukin-1 (IL-1) production<i>in vitro</i>. Enhancement of IL-1 production by interferon (IFN) gamma, tumour necrosis factor-alpha, IL-2 and IL-1, and inhibition by IFN-alpha

Danis, V A; Kulesz, A. J.; Nelson, D. S.; Brooks, P. M.

doi:10.1111/j.1365-2249.1990.tb03306.x

Cited by 50 publications

(15 citation statements)

References 23 publications

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“…This report confirms previous observations (Danis et al, 1990) that low concentrations of certain cytokines, particularly in combination, may stimulate significant production of IL-I by monocytes. Combination of IL-2 with IFN-7 was previously shown to induce IL-I production by monocytes and here we show that this combination also induced TNF-a secretion.…”

Section: Discussionsupporting

confidence: 82%

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Effects of granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-2, interferon-gamma (IFN-γ), tumour necrosis factor-alpha (TNF-α) and IL-6 on the production of immunoreactive IL-1 and TNF-α by human monocytes

Danis

Franic

Rathjen

et al. 1991

Clinical and Experimental Immunology

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SUMMARYThe effects of GM-CSF, IL-2, IFN-y. TNF-a and IL-6 on the production of IL-I (both secreted and cell associated) and TNF-a by peripheral blood monocytes were studied. Monocytes were cultured for 20 h in suspension and in serum-free conditions which minimized background stimulation of monokine production. GM-CSF. IL-2 and TNF-a directly induced the production of cell-associated IL-1 but liUlcornoIL-l or TNF-a secretion. Combination of GM-CSF with !FN-y. IL-2 or TNF-a synergistically enhanced IL-1 secretion and had an additive eflect on cell-associated IL-1 production. Combination of IL-2 with IFN-7 or TNF-a also synergistically enhanced IL-I secretion but theefiect on cell-associated IL-I production was less than additive. GM-CSF synergistically enhaneed TNF-a secretion induced by IFN-y but not by lipopolysaccharide. GM-CSF did not enhanee TNF-a secretion induced by IL-2 or TNF-a. In contrast. IL-2 syncrgisticatly enhanced TNF-a seeretion induced by IFN--/. These results are discussed in relation lo cytokine involvement in rheumatoid arthritis.

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Section: Discussionsupporting

confidence: 82%

“…Monocyte isolation and enrichment were achieved by density gradient and counterflow centrifugation steps as previously described (Danis et at... 1990). Recovery of monocytes was greater than 85' !/ii and purity was greater than %0"A, by the criterion of latex ingestion.…”

Section: Monocyte Isolation and Culturementioning

confidence: 99%

Effects of granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-2, interferon-gamma (IFN-γ), tumour necrosis factor-alpha (TNF-α) and IL-6 on the production of immunoreactive IL-1 and TNF-α by human monocytes

Danis

Franic

Rathjen

et al. 1991

Clinical and Experimental Immunology

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“…Since APCs are a dominant source of IL-1β and IL-23 [24], [25], we wished to establish whether monocytes pulsed with dmLT and PPD could induce increased IL-17A production from CD4+ T cells. Purified CD14+ monocytes were stimulated with PPD alone or in combination with 1 µg/ml dmLT for 24 hours, and the monocytes were then washed thoroughly before CD4+ T cells were added to the cultures, limiting the direct contact between CD4+ cells and dmLT.…”

Section: Resultsmentioning

confidence: 99%

The Adjuvant Double Mutant Escherichia coli Heat Labile Toxin Enhances IL-17A Production in Human T Cells Specific for Bacterial Vaccine Antigens

et al. 2012

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The strong adjuvant activity and low enterotoxicity of the novel mucosal adjuvant double mutant Escherichia coli heat labile toxin, LT(R192G/L211A) or dmLT, demonstrated in mice, makes this molecule a promising adjuvant candidate. However, little is known about the mechanisms responsible for the adjuvant effect of dmLT or whether dmLT also has an adjuvant function in humans.We investigated the effect of dmLT on human T cell responses to different bacterial vaccine antigens: the mycobacterial purified protein derivative (PPD) antigen, tested in individuals previously vaccinated with Bacillus Calmette-Guérin, the LT binding subunit (LTB), evaluated in subjects immunised with oral inactivated whole cell vaccines against enterotoxigenic Escherichia coli, and Streptococcus pneumoniae whole cell vaccine antigens, tested in subjects naturally exposed to pneumococci. We found that dmLT enhanced the production of IL-17A by peripheral blood mononuclear cells in response to all antigens tested. dmLT had comparable effects on IL-17A responses to PPD as the single mutant LT(R192G) adjuvant, which has demonstrated clinical adjuvant activity in humans. Neutralisation of IL-1β and IL-23, but not IL-6, suppressed the IL-17A-enhancing effect of dmLT. Furthermore, CD4+ T cells produced higher levels of IL-17A when stimulated with monocytes pulsed with PPD and dmLT compared to PPD alone, supporting an important role of antigen presenting cells in enhancing IL-17A responses. dmLT also potentiated mitogen-induced IL-17A and IL-13 production. However, dmLT had variable influences on IFN-γ responses to the different stimuli tested.Our demonstration of a potent ability of dmLT to enhance human Th17 type T cell responses to bacterial vaccine antigens encourages further evaluation of the adjuvant function of dmLT in humans.

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“…157 Besides direct regulation of IL-1 protein expression, type I IFNs also potently induce anti-inflammatory IL-1Ra and IL-10, which in turn can inhibit IL-1 signaling effects. 79, 160, 161, 162, 163, 164, 165 In addition, 25-hydroxycholesterol has been implicated as a downstream effector mechanism of type I IFN-mediated inhibition of IL-1β expression and inflammasome activation. 166 More recently, with increased understanding of the complex regulation of IL-1β processing, we now know that type IFNs and IL-10 also potently regulate NLRP1 and NLRP3 inflammasome activation thereby further modulating IL-1 activity.…”

Section: Il-1 and Type I Ifn Cross Talkmentioning

confidence: 99%

Clash of the Cytokine Titans: counter-regulation of interleukin-1 and type I interferon-mediated inflammatory responses

2016

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Over the past decades the notion of ‘inflammation' has been extended beyond the original hallmarks of rubor (redness), calor (heat), tumor (swelling) and dolor (pain) described by Celsus. We have gained a more detailed understanding of the cellular players and molecular mediators of inflammation which is now being applied and extended to areas of biomedical research such as cancer, obesity, heart disease, metabolism, auto-inflammatory disorders, autoimmunity and infectious diseases. Innate cytokines are often central components of inflammatory responses. Here, we discuss how the type I interferon and interleukin-1 cytokine pathways represent distinct and specialized categories of inflammatory responses and how these key mediators of inflammation counter-regulate each other.

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Cytokine regulation of human monocyte interleukin-1 (IL-1) productionin vitro. Enhancement of IL-1 production by interferon (IFN) gamma, tumour necrosis factor-alpha, IL-2 and IL-1, and inhibition by IFN-alpha

Cited by 50 publications

References 23 publications

Effects of granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-2, interferon-gamma (IFN-γ), tumour necrosis factor-alpha (TNF-α) and IL-6 on the production of immunoreactive IL-1 and TNF-α by human monocytes

Effects of granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-2, interferon-gamma (IFN-γ), tumour necrosis factor-alpha (TNF-α) and IL-6 on the production of immunoreactive IL-1 and TNF-α by human monocytes

The Adjuvant Double Mutant Escherichia coli Heat Labile Toxin Enhances IL-17A Production in Human T Cells Specific for Bacterial Vaccine Antigens

Clash of the Cytokine Titans: counter-regulation of interleukin-1 and type I interferon-mediated inflammatory responses

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