Cell-cell contact in chronic inflammation: the importance to cytokine regulation in tissue destruction and repair

Burger, Danielle; Roux‐Lombard, Pascale; Chizzolini, Carlo; Dayer, Jean‐Michel

doi:10.1007/978-3-0348-7883-8_8

Cited by 5 publications

(5 citation statements)

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“…Besides triggering pro-inflammatory cytokine production, contact-mediated activation of monocytes also induces the production and/or shedding of cytokine inhibitors such as the secreted form of IL-1 receptor antagonist (sIL-1Ra), and soluble receptors of IL-1 and TNF [6]–[9]. Once stimulated, most T cell types, including T cell clones, freshly isolated T lymphocytes, and T cell lines such as HUT-78 cells, induce the production of IL-1β and TNF in monocytes/macrophages [10]. Furthermore, depending on T cell type and T cell stimulus, direct cellular contact with stimulated T lymphocytes can induce different patterns of products in monocytes/macrophages (reviewed in [3], [4], [11]), suggesting that multiple ligands and counter-ligands are involved in the contact-mediated activation of monocytes/macrophages.…”

Section: Introductionmentioning

confidence: 99%

HDL Interfere with the Binding of T Cell Microparticles to Human Monocytes to Inhibit Pro-Inflammatory Cytokine Production

et al. 2010

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BackgroundDirect cellular contact with stimulated T cells is a potent mechanism that induces cytokine production in human monocytes in the absence of an infectious agent. This mechanism is likely to be relevant to T cell-mediated inflammatory diseases such as rheumatoid arthritis and multiple sclerosis. Microparticles (MP) generated by stimulated T cells (MPT) display similar monocyte activating ability to whole T cells, isolated T cell membranes, or solubilized T cell membranes. We previously demonstrated that high-density lipoproteins (HDL) inhibited T cell contact- and MPT-induced production of IL-1β but not of its natural inhibitor, the secreted form of IL-1 receptor antagonist (sIL-1Ra).Methodology/Principal FindingsLabeled MPT were used to assess their interaction with monocytes and T lymphocytes by flow cytometry. Similarly, interactions of labeled HDL with monocytes and MPT were assessed by flow cytometry. In parallel, the MPT-induction of IL-1β and sIL-1Ra production in human monocytes and the effect of HDL were assessed in cell cultures. The results show that MPT, but not MP generated by activated endothelial cells, bond monocytes to trigger cytokine production. MPT did not bind T cells. The inhibition of IL-1β production by HDL correlated with the inhibition of MPT binding to monocytes. HDL interacted with MPT rather than with monocytes suggesting that they bound the activating factor(s) of T cell surface. Furthermore, prototypical pro-inflammatory cytokines and chemokines such as TNF, IL-6, IL-8, CCL3 and CCL4 displayed a pattern of production induced by MPT and inhibition by HDL similar to IL-1β, whereas the production of CCL2, like that of sIL-1Ra, was not inhibited by HDL.Conclusions/SignificanceHDL inhibit both MPT binding to monocytes and the MPT-induced production of some but not all cytokines, shedding new light on the mechanism by which HDL display their anti-inflammatory functions.

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Section: Introductionmentioning

confidence: 99%

HDL Interfere with the Binding of T Cell Microparticles to Human Monocytes to Inhibit Pro-Inflammatory Cytokine Production

et al. 2010

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“…Besides triggering proinflammatory cytokine production, contact-mediated activation of monocytes induced the production and/or shedding of cytokine inhibitors such as sIL-1Ra and soluble receptors of IL-1 and TNF [2][3][4][5]. Most T cell types, including T cell clones, freshly isolated T lymphocytes, and T cell lines such as HUT-78 cells, induce IL-1 and TNF in monocytes/macrophages [6]. Furthermore, depending on T cell type and T cell stimulus, direct cell-cell contact with stimulated T lymphocytes can induce different patterns of products in monocytes/ macrophages, as reviewed in refs.…”

Section: Introductionmentioning

confidence: 99%

Stimulated T cells generate microparticles, which mimic cellular contact activation of human monocytes: differential regulation of pro- and anti-inflammatory cytokine production by high-density lipoproteins

Scanu

Molnarfi

Brandt

et al. 2008

Journal of Leukocyte Biology

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Imbalance in cytokine homeostasis plays an important part in the pathogenesis of chronic inflammatory diseases such as multiple sclerosis and rheumatoid arthritis. We demonstrated that T cells might exert a pathological effect through direct cellular contact with human monocytes/macrophages, inducing a massive up-regulation of the prototypical proinflammatory cytokines IL-1beta and TNF. This mechanism that might be implicated in chronic inflammation is specifically inhibited by high-density lipoproteins (HDL). Like many other stimuli, besides proinflammatory cytokines, the contact-mediated activation of monocytes induces the production of cytokine inhibitors such as the secreted form of the IL-1 receptor antagonist (sIL-1Ra). The present study demonstrates that stimulated T cells generate microparticles (MP) that induce the production of TNF, IL-1beta, and sIL-1Ra in human monocytes; the production of TNF and IL-1beta but not that of sIL-1Ra is inhibited in the presence of HDL. The results were similar when monocytes were stimulated by whole membranes of T cells or soluble extracts of the latter. This suggests that MP carry similar monocyte-activating factors to cells from which they originate. Thus, by releasing MP, T cells might convey surface molecules similar to those involved in the activation of monocytes by cellular contact. By extension, MP might affect the activity of cells, which are usually not in direct contact with T cells at the inflammatory site. Furthermore, this study demonstrates that HDL exert an anti-inflammatory effect in nonseptic activation of human monocytes, not only by inhibiting the production of IL-1beta and TNF but also, by leaving sIL-1Ra production unchanged.

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“…The activator(s) of IL-1␤ production in monocytes/macrophages upon chronic/sterile inflammation, i.e., in the absence of bacterial products, remain to be identified, but current evidence suggests that direct cellular contact with stimulated T cells might play a major part in this process, T cells and monocytes/macrophages being in close proximity at the inflammatory site (20). Indeed, contact-mediated activation of human monocytes/macrophages by stimulated T lymphocytes is a potent proinflammatory mechanism that triggers massive up-regulation of proinflammatory cytokine expression (21)(22)(23). T cell contact-mediated activation of monocytes/macrophages by stimulated T cells is comparable to LPS in inducing IL-1␤ and TNF production (24).…”

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confidence: 99%

Opposite Regulation of IL-1β and Secreted IL-1 Receptor Antagonist Production by Phosphatidylinositide-3 Kinases in Human Monocytes Activated by Lipopolysaccharides or Contact with T Cells

Molnarfi

Gruaz

Dayer

et al. 2007

The Journal of Immunology

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The unbalanced production of IL-1β and its natural, specific inhibitor, the secreted IL-1R antagonist (sIL-1Ra), plays an important role in chronic/sterile inflammation. Relevant to this condition is direct cellular contact with stimulated T cells which is a potent inducer of cytokine production in human monocytes/macrophages. We previously demonstrated that activation of PI3Ks is a prerequisite of the transcription of the sIL-1Ra gene in human monocytes activated by IFN-β. In this study, we addressed the question of PI3K involvement in the production of IL-1β and sIL-1Ra in monocytes activated by cellular contact with stimulated T cells (mimicked by CHAPS-solubilized membranes of stimulated T cells (CEsHUT)), and a crude preparation of LPS, to compare stimuli relevant to chronic/sterile and acute/infectious inflammation, respectively. In monocytes activated by either CEsHUT or LPS, the inhibition of PI3Ks abrogated sIL-1Ra transcript expression and sIL-1Ra production, demonstrating that PI3Ks control the induction of sIL-1Ra gene transcription. In contrast, PI3K inhibition increased the production of IL-1β protein in both CEsHUT- and LPS-activated monocytes, the enhancement being drastically higher in the former. This was not due to changes in IL-1β mRNA steady-state levels or transcript stability, but to the involvement of PI3Ks in the repression of IL-1β secretion. The downstream PI3K effector, Akt, was implicated in this process. The present results demonstrate that PI3Ks are involved in the inhibition of IL-1β secretion and in the induction of sIL-1Ra production in human blood monocytes by controlling different mechanisms in conditions mimicking chronic/sterile (CEsHUT) and acute/infectious (LPS) inflammation.

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Cell-cell contact in chronic inflammation: the importance to cytokine regulation in tissue destruction and repair

Cited by 5 publications

References 122 publications

HDL Interfere with the Binding of T Cell Microparticles to Human Monocytes to Inhibit Pro-Inflammatory Cytokine Production

HDL Interfere with the Binding of T Cell Microparticles to Human Monocytes to Inhibit Pro-Inflammatory Cytokine Production

Stimulated T cells generate microparticles, which mimic cellular contact activation of human monocytes: differential regulation of pro- and anti-inflammatory cytokine production by high-density lipoproteins

Opposite Regulation of IL-1β and Secreted IL-1 Receptor Antagonist Production by Phosphatidylinositide-3 Kinases in Human Monocytes Activated by Lipopolysaccharides or Contact with T Cells

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