Transcriptional Regulation of Intracellular IL-1 Receptor Antagonist Gene by IL-1α in Primary Mouse Keratinocytes

La, Eunhye; Fischer, Susan M.

doi:10.4049/jimmunol.166.10.6149

Cited by 26 publications

(14 citation statements)

References 44 publications

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“…There is a selective requirement for the NF-B family member c-Rel in IL-12 p40 gene expression. Alterations in the ratios of NF-B family members (27) may explain a phenomena observed in this study; NO profoundly inhibited IL-12 p40 expression, but other cytokines that are regulated through NF-B, such as IL-1 receptor antagonist (28), were induced normally (data not shown). Activation of NF-B has been well described through MyD88-independent signal transduction pathways (29), which may also explain why all NF-B-regulated genes are not inhibited by NO to the same extent or with the same kinetics as IL-12 p40.…”

Section: Fig 5 No Inhibits Lps-inducible Nf-b Binding To the Il-12 mentioning

confidence: 78%

Inhibition of Interleukin-12 p40 Transcription and NF-κB Activation by Nitric Oxide in Murine Macrophages and Dendritic Cells

Xiong

Zhu

et al. 2004

Journal of Biological Chemistry

104

106

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Nitric oxide (NO), an important effector molecule of the innate immune system, can also regulate adaptive immunity. In this study, the molecular effects of NO on the toll-like receptor signaling pathway were determined using interleukin-12 (IL-12) as an immunologically relevant target gene. The principal conclusion of these experiments is that NO inhibits IL-1 receptor-associated kinase (IRAK) activity and attenuates the molecular interaction between tumor necrosis factor receptor-associated factor-6 and IRAK. As a consequence, the NO donor S-nitroso-N-acetylpenicillamine (

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Section: Fig 5 No Inhibits Lps-inducible Nf-b Binding To the Il-12 mentioning

confidence: 78%

Inhibition of Interleukin-12 p40 Transcription and NF-κB Activation by Nitric Oxide in Murine Macrophages and Dendritic Cells

Xiong

Zhu

et al. 2004

Journal of Biological Chemistry

104

106

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“…Additionally, primary murine keratinocytes have been shown to upregulate icIL-1ra mRNA production following IL-1a exposure in a time-and concentration-dependent manner (La et al, 1999) and transcription factor binding sites on the icIL1ra promoter responsible for this increase, including AP-1, have been identified (La and Fischer, 2001;La et al, 2002). Our findings extend these observations by the demonstration of a concentration-dependent induction of IL-1ra protein release by IL-1a and our observation that IL-1a release Counter-regulation of interleukin-1 receptor antagonist (IL-1ra) release in mice transgenic for IL-1a.…”

Section: Discussionmentioning

confidence: 99%

Counter-Regulation of Interleukin-1α (IL-1α) and IL-1 Receptor Antagonist in Murine Keratinocytes

Mee

Antonopoulos

Poole

et al. 2005

Journal of Investigative Dermatology

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Interleukin-1alpha (IL-1alpha) is a potent proinflammatory cytokine constitutively expressed by keratinocytes, which also synthesize a specific inhibitor of IL-1 activity, intracellular IL-1 receptor antagonist (IL-1ra). Although homeostatic regulation of the IL-1 system in keratinocytes has long been suspected, there is currently little evidence for this. To explore this issue, the PAM212 murine keratinocyte cell line was exposed to increasing concentrations of either IL-1alpha or IL-1ra and the opposing ligand was assessed by ELISA. Release of IL-1ra was induced following stimulation by murine IL-1alpha in a concentration-dependent manner and, conversely, IL-1ra stimulation increased IL-1alpha release. To determine whether a similar homeostatic circuit operates in vivo, epidermis from transgenic mice in which overexpression of IL-1alpha or IL-1ra was targeted to keratinocytes was analyzed. Epidermal sheets derived from IL-1alpha transgenic mice released eight times more IL-1ra than those from wild-type mice following ex vivo culture and similarly, IL-1alpha release was increased 3-4-fold in epidermal sheets derived from IL-1ra transgenic epidermis, Use of specific neutralizing antibodies against type I and type II IL-1 receptors indicated that the counter-regulation mechanism is mediated extracellularly through the type I IL-1 receptor alone. Taken together, these observations provide the first demonstration of mutual counter-regulation of IL-1 receptor ligands in keratinocytes.

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“…Two independent experiments are shown. expression in these cells as it does in other cell types (La and Fischer, 2001). To increase the IL-1Ra/IL-1 ratio, however, additional factors are probably involved.…”

Section: Figurementioning

confidence: 98%

Increased Expression and a Potential Anti-Inflammatory Role of TRAIL in Atopic Dermatitis

Vassina

Leverkus

Yousefi

et al. 2005

Journal of Investigative Dermatology

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The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces apoptosis of many transformed but also of non-transformed cells. In addition, TRAIL receptor activation has been reported to activate non-apoptotic signaling pathways. Here, we report an increased expression of TRAIL in peripheral blood T cells and monocytes from patients with atopic dermatitis (AD) compared with control individuals. High TRAIL expression was also observed in skin-infiltrating T cells of AD patients. Topical tacrolimus treatment reduced the total number of T cells in the skin, but the relative proportion of TRAIL-positive cells within both CD4+ and CD8+ cell populations did not change. TRAIL was demonstrated to induce the expression of interleukin-1 receptor antagonist (IL-1Ra) in keratinocytes in a caspase-independent manner in vitro. Moreover, increased expression of IL-1Ra was observed in keratinocytes of AD lesional skin. These data suggest that TRAIL-expressing inflammatory skin cells may contribute to the epidermal activation of the IL-1Ra gene in AD.

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Transcriptional Regulation of Intracellular IL-1 Receptor Antagonist Gene by IL-1α in Primary Mouse Keratinocytes

Cited by 26 publications

References 44 publications

Inhibition of Interleukin-12 p40 Transcription and NF-κB Activation by Nitric Oxide in Murine Macrophages and Dendritic Cells

Inhibition of Interleukin-12 p40 Transcription and NF-κB Activation by Nitric Oxide in Murine Macrophages and Dendritic Cells

Counter-Regulation of Interleukin-1α (IL-1α) and IL-1 Receptor Antagonist in Murine Keratinocytes

Increased Expression and a Potential Anti-Inflammatory Role of TRAIL in Atopic Dermatitis

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