作者: Jutta Hoeck , Maximilian Woisetschläger
DOI: 10.4049/JIMMUNOL.167.6.3216
关键词:
摘要: Allergic inflammatory conditions such as asthma are characterized by an accumulation of eosinophils at sites inflammation. Eotaxin-3/CCL26 is a member the family CC chemokines, which known to be potent chemoattractants for eosinophils. This chemokine was shown up-regulated IL-4 and IL-13 in endothelial cells. study demonstrates that eotaxin-3 transcription protein expression stimulated time- dose-dependent fashion human dermal fibroblasts. In contrast eotaxin-1/CCL11, TNF-alpha could not act inducer on its own nor did it synergize with IL-4. The activities promoter luciferase constructs were significantly increased effect mediated binding site factor STAT6 sequence. Mutations abrogated up-regulation activity. STAT6-defective embryonic kidney 293 cells, wild-type construct, but mutant, inducible only upon cotransfection vector. addition, detectable supernatants STAT6-transfected cells or stimulation. same experiments, induced activation monocyte chemoattractant protein-1/CCL2 gene independent transfection. These results indicate activate STAT6-dependent fashion. Although both eotaxin-1 -3 regulated this factor, response stimulation appears different.