کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9236699 | 1207486 | 2005 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Increased expression of soluble decoy receptor 3 in acutely inflamed intestinal epithelia
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کلمات کلیدی
LTAMEKKTNFc-Jun NH2-terminal protein kinaseDC2DcR3TL1AT helperTNFRTLRLPSJnkDC1ERKMAPK - MAPKAppendix - آپاندیسlipoteichoic acid - اسید لیپتویکوئیکinflammation - التهاب( توروم) Toll-like receptor - تیالآرintestinal epithelial cell - سلول های اپیتلیال رودهFas Ligand - فاس لیگاندFasL - فاسدtumor necrosis factor - فاکتور نکروز تومورlipopolysaccharide - لیپوپلی ساکاریدMEK - مجاهدین خلقlight - نور mitogen-activated protein kinase - پروتئین کیناز فعال با mitogenIEC - کمیسیون مستقل انتخاباتextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولیTNF receptor - گیرنده TNFDecoy receptor 3 - گیرنده طعمه 3
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Increased expression of soluble decoy receptor 3 in acutely inflamed intestinal epithelia Increased expression of soluble decoy receptor 3 in acutely inflamed intestinal epithelia](/preview/png/9236699.png)
چکیده انگلیسی
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.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Clinical Immunology - Volume 115, Issue 3, June 2005, Pages 286-294
Journal: Clinical Immunology - Volume 115, Issue 3, June 2005, Pages 286-294
نویسندگان
Sunghee Kim, Anastasia Fotiadu, Vassiliki Kotoula,