ORIGINAL ARTICLESRegulatory mechanisms of Th2 cytokine–induced eotaxin-3 production in bronchial epithelial cells: possible role of interleukin 4 receptor and nuclear factor–κB
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An emerging role for eotaxins in neurodegenerative disease
2018, Clinical ImmunologyCitation Excerpt :A growing body of evidence also identifies tissue resident macrophages in the lung and intestinal tract as an important source of these mediators [27,28], while scattered papers demonstrate CCL11 production by cells such as adipocytes and chondrocytes [29,30]. Largely based on in vitro experimentation, inflammatory mediators known to induce eotaxin family members in lung epithelial cells or tissue fibroblasts include the Th2-associated cytokines, interleukin (IL)-4 and IL-13, bacterial lipopolysaccharide (LPS), tumor necrosis factor (TNF)-α, and histamine [26,31–34], while known suppressors include dexamethasone, Th1-associated interferon (IFN)-γ, IL-17, bisphosphonates, β2 adrenergic receptor agonists and fumaric acid [23,35–39]. In sum, eotaxins are produced by a wide range of cell types and appear to be under dynamic control of multiple inflammatory mediators.
Effect of San-ao Decoction, a traditional Chinese prescription, on IL-4 treated normal human bronchial epithelium
2010, Journal of EthnopharmacologyChemokines
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This study was supported in part by grant C2–14570753 from the Ministry of Education, Science, Sports, and Culture of Japan.