MAPK/ERK通路
Fas配体
肿瘤坏死因子α
受体
激酶
细胞生物学
信号转导
细胞凋亡
脂多糖
肠上皮
诱饵
化学
生物
癌症研究
免疫学
上皮
程序性细胞死亡
生物化学
遗传学
作者
Sunghee Kim,Anastasia Fotiadu,Vassiliki Kotoula
标识
DOI:10.1016/j.clim.2005.02.014
摘要
Decoy receptor 3 (DcR3), a soluble receptor in the tumor necrosis factor (TNF) receptor family, is known to inhibit apoptosis mediated by pro-apoptotic TNF family cytokines such as Fas ligand (FasL), TL1A, and LIGHT. Therefore, the regulation of DcR3 expression under certain pathophysiological conditions is of interest since the level of soluble DcR3 would most likely affect the homeostasis of cells and tissues. We found that human intestinal epithelial cell (IEC) lines (SW480, SW620, and HT29) could selectively increase DcR3 release in response to lipopolysaccharide (LPS) and that all the cells preferentially expressed Toll-like receptor 4 (TLR-4). LPS-induced DcR3 releases in IECs appeared to be via the activation of mitogen-activated protein kinases (MAPK) such as extracellular signal-regulated kinase 1 and 2 (ERK1/2) and c-Jun NH2-terminal protein kinase (JNK), and the transcription factor NF-κB. Moreover, the increased expression of DcR3 in appendix epithelia from patients with acute appendicitis was demonstrated. Taken together, the results indicated that DcR3 might play an important role in the human intestinal epithelium during acute inflammatory processes caused by endotoxin challenge.
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