High intestinal and systemic levels of decoy receptor 3 (DcR3) and its ligand TL1A in active ulcerative colitis

Copyright © 2010 Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 137(2010), 2 vom: 01. Nov., Seite 242-9
1. Verfasser: Bamias, Giorgos (VerfasserIn)
Weitere Verfasser: Kaltsa, Garyfallia, Siakavellas, Spyros I, Papaxoinis, Kostis, Zampeli, Evanthia, Michopoulos, Spyros, Zouboulis-Vafiadis, Irene, Ladas, Spiros D
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2010
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Receptors, Tumor Necrosis Factor, Member 6b Tumor Necrosis Factor Ligand Superfamily Member 15 Tumor Necrosis Factor-alpha C-Reactive Protein 9007-41-4
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100 1 |a Bamias, Giorgos  |e verfasserin  |4 aut 
245 1 0 |a High intestinal and systemic levels of decoy receptor 3 (DcR3) and its ligand TL1A in active ulcerative colitis 
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520 |a Decoy receptor-3 (DcR3) is a member of the TNF receptor superfamily of proteins, which has been implicated in anti-apoptotic and anti-inflammatory pathways, via binding to TL1A, LIGHT and Fas-L. The role of the TL1A/DcR3 ligand/receptor pair in ulcerative colitis (UC) has not been studied. We investigated the systemic (peripheral blood) and local (large intestine) expression of DcR3 and TL1A in 64 patients with UC and 56 healthy controls. DcR3 serum concentrations were highly elevated in patients with active UC (P<0.0001 vs. healthy controls). This elevation was clearly related to the presence of intestinal inflammation as it was less frequently observed in patients in remission (P=0.003 vs. active UC) whereas effective treatment resulted in disappearance or significant decrease of serum DcR3 (P=0.006 vs. pre-treatment). Furthermore, DcR3 mRNA transcripts were significantly elevated in inflamed areas of the colon (P=0.002 vs. non-affected of the same patient). In addition to DcR3 elevation, we found increased circulating levels of TL1A in patients with either active or inactive UC in comparison to healthy controls (P<0.001 for both). We conclude that elevated serum DcR3 may serve as an indicator of active colonic inflammation in patients with UC. TL1A/DcR3-mediated pathways may participate in the pathogenesis of UC 
650 4 |a Journal Article 
650 7 |a Receptors, Tumor Necrosis Factor, Member 6b  |2 NLM 
650 7 |a Tumor Necrosis Factor Ligand Superfamily Member 15  |2 NLM 
650 7 |a Tumor Necrosis Factor-alpha  |2 NLM 
650 7 |a C-Reactive Protein  |2 NLM 
650 7 |a 9007-41-4  |2 NLM 
700 1 |a Kaltsa, Garyfallia  |e verfasserin  |4 aut 
700 1 |a Siakavellas, Spyros I  |e verfasserin  |4 aut 
700 1 |a Papaxoinis, Kostis  |e verfasserin  |4 aut 
700 1 |a Zampeli, Evanthia  |e verfasserin  |4 aut 
700 1 |a Michopoulos, Spyros  |e verfasserin  |4 aut 
700 1 |a Zouboulis-Vafiadis, Irene  |e verfasserin  |4 aut 
700 1 |a Ladas, Spiros D  |e verfasserin  |4 aut 
773 0 8 |i Enthalten in  |t Clinical immunology (Orlando, Fla.)  |d 1999  |g 137(2010), 2 vom: 01. Nov., Seite 242-9  |w (DE-627)NLM098196855  |x 1521-7035  |7 nnns 
773 1 8 |g volume:137  |g year:2010  |g number:2  |g day:01  |g month:11  |g pages:242-9 
856 4 0 |u http://dx.doi.org/10.1016/j.clim.2010.07.001  |3 Volltext 
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