TARC augments TNF‐α‐induced CTACK production in keratinocytes

Vestergaard, Christian; Johansen, Claus; Christensen, Ulla; Just, Helle; Hohwy, Thomas; Deleuran, Mette

doi:10.1111/j.0906-6705.2004.00202.x

Cited by 26 publications

(21 citation statements)

References 28 publications

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“…A recent report revealed that TARC/CCL17, a ligand for CCR4, is significantly elevated in MF patients' serum, and that this is correlated with clinical and disease stages (19). It is also reported that TARC/CCL17 augments CTACK/CCL27 expression through tumor necrosis factor-a in atopic skin (20). These findings account for our observations that serum CTACK/CCL27 levels are elevated in patients with MF in accordance with the advance of the clinical stage.…”

Section: Discussionsupporting

confidence: 87%

Presence of Circulating CCR10+ T cells and Elevated Serum CTACK/CCL27 in the Early Stage of Mycosis Fungoides

Fujita

Abe

Sasaki

et al. 2006

Clinical Cancer Research

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Purpose: Mycosis fungoides (MF), a common type of cutaneous T cell lymphoma with an indolent clinical course, has the characteristic that malignant T cell clones are recruited into the skin from the early disease stages. The mechanisms of recruitment have been suggested from our knowledge of various chemokine-chemokine receptor interactions. Recently, CCR10 and CTACK/CCL27 were proposed to play a role in the recruitment of other types of cutaneous T cell lymphoma. We examined the expression of CCR10 in peripheral blood and serum CTACK/CCL27 levels in patients with MF. Experimental Design: Eighteen patients with MF, six patients with atopic dermatitis, and nine healthy volunteers were enrolled in our investigation. We investigated the differences in CCR10+ CD4+ expression in peripheral blood mononuclear cells by flow cytometry. Serum CTACK/CCL27 levels were determined using a CTACK/CCL27 ELISA assay kit. Results: The number of circulating CCR10+ CD4+ cells was significantly higher in MF peripheral blood than in controls, even during the early stages. In lesional MF skin, infiltrating tumor cells also showed extensive expression of CCR10. The serum level of CTACK/CCL27 was higher in patients with MF than normal controls, but no statistical difference was found compared with atopic dermatitis patients. Conclusions: CCR10-CTACK/CCL27 interactions between circulating T cells and keratinocytes would seem to play an important role in the pathophysiology of MF from the early disease stages.

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Section: Discussionsupporting

confidence: 87%

Presence of Circulating CCR10+ T cells and Elevated Serum CTACK/CCL27 in the Early Stage of Mycosis Fungoides

Fujita

Abe

Sasaki

et al. 2006

Clinical Cancer Research

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“…Cells were treated with various concentrations of RuCO as exogenous CO donor for 30 min and then with and without IFN-γ (10 ng/mL) and TNF-α (10 ng/mL) for 9 h. Total RNAs were extracted and chemokines expression were subjected for RT-PCR analysis. (Vestergaard et al, 2000(Vestergaard et al, , 2004. Recently, Frukawa et al (2004) also reported that PBMC from atopic dermatitis patients produces TARC/CCL17 in response to dust-mite allergens, which are well-known environmental allergens.…”

Section: Discussionmentioning

confidence: 99%

“…CTACK/CCL27 also is highly expressed in the basal epidermis of lesioned skin of NC/ Nga mice, which are regarded to be a mouse model of human AD, and CTACK/CCL27 expression in the basal epidermis disappears as the lesion heals (Vestergaard et al, 1999). Furthermore, Vestergaard et al (2000Vestergaard et al ( , 2004 reported that CATCK/CCL27 is expressed in HaCaT cells when the cells are stimulated with TNF-α and was a major regulator of keratinocyte precursor cell migration from the bone marrow to the skin. CTACK/CCL27 is pivotal in mediating the migration of CLA + lymphocytes into the skin.…”

Section: Discussionmentioning

confidence: 99%

“…It has also been reported that the peripheral immune responses of AD patients are skewed to a Th2 dominant bias. Th2 chemokines are overexpressed by keratinocytes, especially, epidermis in atopic dermatitis lesions in both murine model and atopic dermatitis patients (Horikawa et al, 2002;Sumiyoshi et al, 2003;Vestergaard et al, 2004;Nakazato et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

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Prenylated chalcone from Sophora flavescens suppresses Th2 chemokine expression induced by cytokines via heme oxygenase-1 in human keratinocytes

Choi

Lee

et al. 2010

Arch. Pharm. Res.

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We recently reported the inhibitory effect of an oral administration of a Sophora flavescens Aiton methanol extract on the development of atopic dermatitis in the NC/Nga model mice. Heme oxygenase (HO)-1 has recently emerged as an important cytoprotective enzyme against oxidative stress and inflammatory responses in many cell types. The aim of this study was to investigate the possible mechanism by which prenylated chalcone (PC, 7,9,2',4'-tetrahydroxy-8-isopentenyl-5-methoxychalcone), a natural product isolated from S. flavescens, inhibited cytokine-induced Th2 chemokine expression in human keratinocytes, HaCaT cells. The level of chemokine expression was measured by reverse transcription-polymerase chain reaction and HO-1 study was performed by Western blot analysis. Interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha)-induced thymus- and activation-regulated chemokine (TARC/CCL17), macrophage-derived chemokine (MDC/CCL22), cutaneous T-cell attracting chemokine (CTACK/CCL27) expression in a dose-dependent manner. Interestingly, PC significantly suppressed IFN-gamma and TNF-alpha-induced TARC/CCL17, MDC/CCL22 and CTACK/CCL27 expression via the induction of heme oxygenase (HO)-1. This suppression was completely restored by HO-1 siRNA, suggesting a direct role of HO-1 for the suppressive effect. Furthermore, exogenous CO, but not other end products of HO-1 activity, also suppressed IFN-gamma and TNF-alpha-induced TARC/CCL17, MDC/CCL22 and CTACK/CCL27 expression. These results demonstrate that prenylated chalcone induces HO-1 expression, which in turn HO-1 and/or CO suppresses Th2 chemokine expressions induced by cytokines in human HaCaT cells.

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“…TNF is a major proinflammatory cytokine that is thought to be important in the pathogenesis of asthma [12], food allergy [13,14], ocular allergy [15], and atopic dermatitis [16]. It has been reported that increased number of TNF expressing cells and levels of TNF are observed in the bronchoalveolar lavage (BAL) and in the airways of asthmatics [17], respectively.…”

Section: Introductionmentioning

confidence: 99%

TNF Increases Expression of IL-4 and PARs in Mast Cells

Zhang

Yang²,

He³

2010

Cell Physiol Biochem

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Tumor necrosis factor (TNF) is a proinflammatory cytokine which has been shown to be actively involved in the pathogenesis of allergic inflammation. However, little is known of the effects of TNF on cytokine secretion and protease activated receptor (PAR) expression in mast cells. In the present study, we examined potential influence of TNF on IL-4 and IL-12 release from P815 cells and PAR expression in P815 cells by using flow cytometry analysis, quantitative real time PCR, ELISA and cellular activation of signaling ELISA (CASE) techniques. The results showed that TNF induced up to 2.7-fold increase in IL-4, but not IL-12 release from P815 cells, and PAR-2 antagonist peptide FSLLRY-NH₂ and PAR-4 antagonist peptide trans-cinnamoyl (tc)-YPGKF-NH₂ did not affect TNF induced IL-4 release. Approximately up to 2.4 and 2.3 fold increases in expression of PAR-2 and PAR-4 were observed when cells were incubated with TNF. Pretreatment of cells with TNF for 60 min enhanced trypsin and tryptase induced PAR-2 expression by 2.4 and 2.3 fold; PAR-3 expression by 1.6 and 1.7 fold and PAR-4 expression by 1.6 and 1.7 fold, respectively. LY294002, an inhibitor PI3K abolished TNF induced IL-4 release and phosphorylation of Akt in P815 cells, indicating Akt cell signalling pathway is involved in the event. In conclusion, TNF can stimulate IL-4 release from mast cells through an Akt cell signalling pathway dependent, but PAR independent mechanism. TNF may serve as a regulator for IL-4 production and PAR expression, and through which participates in the mast cell related inflammation.

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TARC augments TNF‐α‐induced CTACK production in keratinocytes

Cited by 26 publications

References 28 publications

Presence of Circulating CCR10+ T cells and Elevated Serum CTACK/CCL27 in the Early Stage of Mycosis Fungoides

Presence of Circulating CCR10+ T cells and Elevated Serum CTACK/CCL27 in the Early Stage of Mycosis Fungoides

Prenylated chalcone from Sophora flavescens suppresses Th2 chemokine expression induced by cytokines via heme oxygenase-1 in human keratinocytes

TNF Increases Expression of IL-4 and PARs in Mast Cells

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