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CCL26 — IL4

Text-mined interactions from Literome

Hoeck et al., J Immunol 2001 : This study demonstrates that eotaxin-3 transcription and eotaxin-3 protein expression are stimulated by IL-4 and IL-13 in a time- and dose dependent fashion in human dermal fibroblasts ... These results indicate that IL-4 and IL-13 activate eotaxin-3 gene expression in a STAT6 dependent fashion
Litterst et al., J Biol Chem 2002 : Importantly, mutagenesis of the STAT-LXXLL motif strongly diminished the IL-4 regulated activation of the endogenous STAT6 target gene eotaxin-3
Yamamoto et al., Am J Respir Cell Mol Biol 2004 : Upregulation of interleukin-4 receptor by interferon-gamma : enhanced interleukin-4 induced eotaxin-3 production in airway epithelium
Kobayashi et al., Ann Allergy Asthma Immunol 2004 : A consistent 10-fold difference in the potency of IL-13- and IL-4 mediated induction of eotaxin-3 mRNA expression was observed ... Pretreatment with tumor necrosis factor a enhanced IL-4 induced eotaxin-1, but not eotaxin-3 , mRNA expression ... These results suggest that differences in the potency of IL-13- and IL-4 mediated induction of eotaxin-3 might be explained by expression of types 1 and 2 IL-4 receptors in bronchial epithelium
Hebenstreit et al., Mol Immunol 2005 : IL-4/IL-13 induced activation of the Eotaxin-3/CCL26 gene in human dermal fibroblasts was shown to be a STAT6 dependent process mediated by a single STAT6 binding motif located upstream of the transcription initiation site
Abonyo et al., Am J Physiol Lung Cell Mol Physiol 2005 (Pneumonia) : On the other hand, anti-CCR3 pretreatment reduced IL-4+IL-13 dependent CCL26 secretion, implying autoregulation
Blanchard et al., Int J Biochem Cell Biol 2005 (Inflammation) : Eotaxin-3/CCL26 gene expression in intestinal epithelial cells is up-regulated by interleukin-4 and interleukin-13 via the signal transducer and activator of transcription 6
Tsuji et al., Eur Respir J 2005 (Respiratory Tract Infections...) : This was reversed by the addition of anti-IL-4Ralpha antibody, suggesting the role of an increased number of IL-4 receptors in enhanced IL-4 induced eotaxin-3 production ... In conclusion, these results suggest that viral airway infection may enhance interleukin-4 induced eotaxin-3 production through upregulation of the interleukin-4 receptor in airway epithelial cells
van Wetering et al., Mol Immunol 2007 : Epithelial differentiation is a determinant in the production of eotaxin-2 and -3 by bronchial epithelial cells in response to IL-4 and IL-13 ... Mucociliary differentiated ALI-cultures expressed and released more eotaxin-3 upon stimulation with IL-4/IL-13 , whereas eotaxin-2 production was predominantly found in squamous differentiated ALI-cultures
Rokudai et al., Biol Pharm Bull 2006 (Asthma...) : Differential regulation of eotaxin-1/CCL11 and eotaxin-3/CCL26 production by the TNF-alpha and IL-4 stimulated human lung fibroblast ... We observed that a human lung fibroblast, HFL-1 produces eotaxin-1 and -3 in response to TNF-alpha plus IL-4 stimulation, accompanied with NF-kappaB and STAT6 activation
Igawa et al., Allergy 2006 (Dermatitis...) : Dermal fibroblasts produced eotaxin and eotaxin-3 in response to stimulation by interleukin (IL)-4 and/or tumor necrosis factor-alpha
Odaka et al., Int Arch Allergy Immunol 2007 : The Th2 cytokine IL-4 preferentially stimulated the expression of the CC chemokine receptor (CCR) 3-ligand chemokines eotaxin, eotaxin-3 , and MCP-4
Nishi et al., Biochem Biophys Res Commun 2008 (Dermatitis, Atopic) : This study investigated the effects of IFN-gamma on IL-4 induced production of eotaxin-3/CCL26 , a potent chemoattractant to eosinophils, in normal human epidermal keratinocytes ( NHEK ) ... When the cells were stimulated with IL-4 and IFN-gamma simultaneously, IL-4 induced CCL26 production was attenuated ... In contrast, prior stimulation with IFN-gamma enhanced IL-4 induced CCL26 production ... These results indicate that IFN-gamma has opposite effects on IL-4 induced CCL26 production in NHEK depending on the time of exposure
Errahali et al., J Interferon Cytokine Res 2009 (Asthma) : Results demonstrate that CCL26-siRNA treatments decreased interleukin-4 induced CCL26 and CCL24 expression by > 70 %
Lalaker et al., American journal of rhinology & allergy 2009 (Ethmoid Sinusitis...) : Expression of eotaxin-3 was stimulated by IL-4 and further enhanced with the addition of DMA
Stubbs et al., Immunology 2010 : By contrast, pretreatment with IFN-gamma decreased total STAT6 protein, blocked IL-4 mediated STAT6 phosphorylation and decreased IL-4 mediated CCL26 mRNA expression and protein release ... These data show that IL-4 and pro-inflammatory cytokines such as TNF-alpha, IL-1beta and IFN-gamma regulate CCL26 synthesis in human monocytic cells, which may be important in regulating monocyte inflammatory responses
Hurst et al., Mol Nutr Food Res 2010 (Asthma) : Since IL-4 stimulated eotaxin-3 ( CCL26 ) secretion is a major factor in the continuous eosinophil recruitment observed in atopic asthma, our focus was to evaluate the effectiveness of blackcurrant polyphenolic compounds on CCL26 secretion in human alveolar epithelial cells ... Furthermore pre-incubation of cells with BC-P caused a time dependent suppression of IL-4 stimulated CCL26 secretion ... Moreover, epigallocatechin ( EGC ), and to a lesser extent epicatechin, metabolites identified in the proanthocyanidin extract, suppressed IL-4 stimulated CCL26 secretion ... Furthermore, both BC-P and purified EGC potentiated the ability of IFN-gamma to suppress IL-4 stimulated CCL26 secretion
Cheng et al., Gut 2013 (Eosinophilic Esophagitis...) : In EoE and GORD cell lines, IL-4 and IL-13 activated the eotaxin-3 promoter, and significantly increased eotaxin-3 mRNA and protein expression
Provost et al., PloS one 2012 (Asthma...) : IL-4 and IL-13 induced the release of eotaxin-3 by airway epithelial cells
Zhang et al., PloS one 2012 (Eosinophilic Esophagitis) : The objective of this study was to elucidate molecular mechanisms underlying PPI inhibition of IL-4 stimulated eotaxin-3 production by esophageal cells ... Omeprazole in concentrations =5 µM significantly decreased IL-4 stimulated eotaxin-3 protein secretion and mRNA expression ... PPIs, in concentrations achieved in blood with conventional dosing, significantly inhibit IL-4 stimulated eotaxin-3 expression in EoE esophageal cells and block STAT6 binding to the promoter
Takahashi et al., Clin Exp Immunol 2013 (Inflammatory Bowel Diseases) : Colonic myofibroblasts were identified as a major source of eotaxin-3 in the colonic mucosa, and interleukin (IL)-4 and IL-13 enhanced eotaxin-3?mRNA and protein expression significantly in these cells