References of "Cleynen, I"
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See detailGenetic and functional evidence for a role of CYLD in Crohn’s Disease: results from a European consortium
Cleynen, I; Vazeille, E; Artieda, M et al

in Journal of Crohn’s and Colitis [=JCC] (2012, February)

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See detailMultiple functional variants at the 3p21 locus contribute to ulcerative colitis: Results from a European consortium
Cleynen, I; Artieda, M; Verspaget, H et al

in Journal of Crohn’s and Colitis [=JCC] (2012, February)

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See detailLong term evolution and impact of immunomodulator cotreatment and withdrawal on infliximab on trough levels in 223 patients with Crohn's disease
Drobne, D; Bossuyt, P; Breynaert, C et al

in Journal of Crohn’s and Colitis [=JCC] (2011)

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See detailThe protease genes CYLD and USP40 are associated with Crohn's disease: results from a European Consortium
Cleynen, I; Artieda, M; Szczyoiorska, M et al

in Gastroenterology (2011), 140(5), 269

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See detailAnti-TNF induced skin manifestations in IBD patients: characterization and search for predisposing factors
Cleynen, I; Van Moerkercke, W; Vande Casteele, N et al

in Acta Gastro-Enterologica Belgica (2011), 74

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See detailEffects of haptoglobin polymorphisms and deficiency on susceptibility to inflammatory bowel disease and on severity of murine colitis.
Marquez, L.; Shen, C.; Cleynen, I. et al

in Gut (2011), 61(4), 528-534

BackgroundHaptoglobin (Hp) is a haemoglobin-binding protein with immunomodulatory properties. Its gene (16q22) harbours a common polymorphism with two different alleles: Hp1 and Hp2. Genotype Hp22 has ... [more ▼]

BackgroundHaptoglobin (Hp) is a haemoglobin-binding protein with immunomodulatory properties. Its gene (16q22) harbours a common polymorphism with two different alleles: Hp1 and Hp2. Genotype Hp22 has been shown to be over-represented in different immune diseases. Results in Crohn's disease (CD) are contradictory.AimsTo determine whether Hp plays a role in inflammatory bowel disease, both genetically and functionally.Methods1061 patients with CD, 755 with ulcerative colitis (UC) and 152 with primary sclerosing cholangitis, as well as 452 healthy controls, were genotyped using touch-down PCR. To confirm association results, 464 CD trios and 151 UC trios were genotyped. Serum Hp concentrations were determined in 62 individuals of different genotype. Colitis was induced in mice with dextran sulphate sodium (DSS) and oxazolone (Oxa). Cytokine production was evaluated by mRNA quantification in colonic tissue and ELISA on supernatants of mesenteric lymph node cells.ResultsPrevalence of Hp2 was higher in CD and UC than in controls. In the confirmatory cohorts, Hp2 was over-transmitted to the affected offspring. Serum Hp concentrations were higher in individuals with genotypes Hp11 and Hp21 than in those with Hp22 (1.38 vs 0.89 g/l). DSS- and Oxa-induced colitis were more severe in Hp-deficient mice than in control mice and accompanied by higher concentrations (although not statistically significantly different) of tissue mRNA for cytokines. Interleukin-17 production was significantly higher in the presence of Hp-deficient serum compared with wild-type serum.ConclusionsThe Hp gene may play a role in susceptibility to inflammatory bowel disease. Its implication in other immune diseases underscores the common pathways between these diseases. Experimental models of colitis showed that Hp has a protective role in inflammatory colitis, most likely by inhibiting the production of Th1 and Th17 cytokines. [less ▲]

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See detailMolecular Reclassification of Crohn’s Disease by cluster analysis of genetic variants.
Cleynen, I.; Mahachie John, Jestinah ULg; Henckaerts, L. et al

in Gastroenterology (2010)

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See detailMolecular Reclassification of Crohn’s Disease by cluster analysis of genetic variants.
Cleynen, I.; Mahachie John, Jestinah ULg; Henckaerts, Liesbet et al

in Acta Gastro-Enterologica Belgica (2010)

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See detailKinetics of C-Reactive Protein (CRP) following maintenance infliximab treatment in Crohn's disease identifies profiles of patients with better outcome
Jürgens, M.; Mahachie John, Jestinah ULg; Cleynen, I. et al

in Gastroenterology (2010), 138(5 (Suppl I)), -686

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See detailCluster analysis of genetic variants enables reclassification of Crohn’s disease at the molecular level
Cleynen, I.; Van Moerkercke, W.; Mahachie John, Jestinah ULg et al

in Gut (2009)

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See detailMucosal Gene Expression of Antimicrobial Peptides in Inflammatory Bowel Disease Before and After First Infliximab Treatment
Arijs, I.; De Hertogh, G.; Lemaire, K. et al

in PLoS ONE (2009), 4(11), 7984

Background: Antimicrobial peptides (AMPs) protect the host intestinal mucosa against microorganisms. Abnormal expression of defensins was shown in inflammatory bowel disease (IBD), but it is not clear ... [more ▼]

Background: Antimicrobial peptides (AMPs) protect the host intestinal mucosa against microorganisms. Abnormal expression of defensins was shown in inflammatory bowel disease (IBD), but it is not clear whether this is a primary defect. We investigated the impact of anti-inflammatory therapy with infliximab on the mucosal gene expression of AMPs in IBD. Methodology/Principal Findings: Mucosal gene expression of 81 AMPs was assessed in 61 IBD patients before and 4-6 weeks after their first infliximab infusion and in 12 control patients, using Affymetrix arrays. Quantitative real-time reverse-transcription PCR and immunohistochemistry were used to confirm microarray data. The dysregulation of many AMPs in colonic IBD in comparison with control colons was widely restored by infliximab therapy, and only DEFB1 expression remained significantly decreased after therapy in the colonic mucosa of IBD responders to infliximab. In ileal Crohn's disease (CD), expression of two neuropeptides with antimicrobial activity, PYY and CHGB, was significantly decreased before therapy compared to control ileums, and ileal PYY expression remained significantly decreased after therapy in CD responders. Expression of the downregulated AMPs before and after treatment (DEFB1 and PYY) correlated with villin 1 expression, a gut epithelial cell marker, indicating that the decrease is a consequence of epithelial damage. Conclusions/Significance: Our study shows that the dysregulation of AMPs in IBD mucosa is the consequence of inflammation, but may be responsible for perpetuation of inflammation due to ineffective clearance of microorganisms. [less ▲]

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See detailMolecular Reclassification of Crohn’s Disease by cluster analysis of genetic variants
Cleynen, I.; Mahachie John, Jestinah ULg; Henkaerts, L. et al

in Gut (2009)

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See detailLong-term efficacy of infliximab and colectomy-free survival in outpatients with refractory ulcerative colitis.
Ferrante, M.; Vermeire, S.; Schnitzler, F. et al

in Journal of Crohn’s and Colitis [=JCC] (2008), 2(1), 3

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See detailDevelopment of psoriasiform skin lesions under anti-TNF therapy: a genetic link?
Cleynen, I.; Claes, B.; Nuytten, H. et al

in Conference Abstract Book (2008)

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See detailGenetic markers and the risk of complicated disease behaviour in Crohn's disease patients
Henckaerts, L.; Cleynen, I.; Joossens, M. et al

in Gastroenterology (2008), 134(4), 349-349

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