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CCL26 — IL13

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
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 ... 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
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
Syed et al., Biomarkers 2007 (Asthma) : A follow-up study in PBMCs from five additional healthy donors showed that the neutralization of IL-13 completely blocked IL-13 induced TARC, MDC and eotaxin 3 production at the protein level
Caldwell et al., J Allergy Clin Immunol 2010 (Eosinophilia...) : FKBP51 overexpression reduced FP action as assessed by FP inhibition of IL-13 induced eotaxin-3 promoter activity
Reh et al., American journal of rhinology & allergy 2010 (Chronic Disease...) : HGF significantly blocked IL-13 induced expression of eotaxin-3 in control SNECs, but not in SNECs derived from CRSwNP subjects ... In patients with CRSwNP, SNECs are resistant to this attenuation, showing continued IL-13 induced eotaxin-3 expression despite HGF treatment
Lim et al., J Biol Chem 2011 : Furthermore, the CRE binding protein binding protein ( CBP ), a histone acetyltransferase, induced base-line and IL-13 induced eotaxin-3 promoter activity
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
Josephson et al., Am J Physiol Lung Cell Mol Physiol 2012 (Asthma...) : Supporting this concept, extended studies demonstrated that 1 ) IL-13 treated tracheal epithelium and peripheral lung tissues exhibit upregulated 11ß-HSD2 activity, 2 ) the latter impairs cortisone induced cortisol accumulation and the ability of administered cortisol to prevent both IL-13 induced heightened airway contractility and eotaxin-3 release from epithelial cells, and 3 ) these proasthmatic responses are prevented by cortisol administration in the presence of 11ß-HSD2 inhibition
Provost et al., PloS one 2012 (Asthma...) : IL-4 and IL-13 induced the release of eotaxin-3 by airway epithelial cells ... LTD ( 4 ) weakly induced the release of eotaxin-3 but clearly potentiated the IL-13 induced eotaxin-3 release
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 ... Interferon ( IFN ) -? acts as a negative regulator on the IL-4- and IL-13 induced eotaxin-3 expression via STAT-1 activation