Abstract | PURPOSE OF REVIEW: RECENT FINDINGS: TL1A may induce IFN-γ-mediated and IL-17-mediated proinflammatory pathways in IBDs by acting on DR3-expressing, CD4(+)CD161(+) lymphocytes, which are substantially enriched at the inflamed intestinal mucosa. In addition, TL1A/DR3 signaling results in expansion of the Treg pool with concomitant and transient inhibition of their suppressive function. Constitutive expression of TL1A in transgenic mice was associated with small intestinal inflammation, which was accompanied by colonic fibrosis both spontaneously and under colitogenic conditions. Recent human studies demonstrated that soluble TL1A and DcR3 are present in the systemic circulation in patients with active IBD and decline after successful anti-inflammatory treatment. SUMMARY:
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Authors | Giorgos Bamias, Li-Guo Jia, Fabio Cominelli |
Journal | Current opinion in gastroenterology
(Curr Opin Gastroenterol)
Vol. 29
Issue 6
Pg. 597-602
(Nov 2013)
ISSN: 1531-7056 [Electronic] United States |
PMID | 24100723
(Publication Type: Journal Article, Review)
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Chemical References |
- Biomarkers
- Cytokines
- Inflammation Mediators
- Receptors, Tumor Necrosis Factor, Member 25
- Tumor Necrosis Factor Ligand Superfamily Member 15
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Topics |
- Animals
- Biomarkers
(blood)
- Cytokines
(biosynthesis)
- Fibrosis
(immunology)
- Humans
- Inflammation Mediators
(immunology)
- Inflammatory Bowel Diseases
(immunology)
- Receptors, Tumor Necrosis Factor, Member 25
(immunology)
- T-Lymphocytes, Regulatory
(immunology)
- Tumor Necrosis Factor Ligand Superfamily Member 15
(immunology)
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