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4 results on '"Crusius, J. Bart A."'

1. Major histocompatibility complex associations of ankylosing spondylitis are complex and involve further epistasis with ERAP1.

Author

Cortes, Adrian, Pulit, Sara L, Leo, Paul J, Pointon, Jenny J, Robinson, Philip C, Weisman, Michael H, Ward, Michael, Gensler, Lianne S, Zhou, Xiaodong, Garchon, Henri-Jean, Chiocchia, Gilles, Nossent, Johannes, Lie, Benedicte A, Førre, Øystein, Tuomilehto, Jaakko, Laiho, Kari, Bradbury, Linda A, Elewaut, Dirk, Burgos-Vargas, Ruben, Stebbings, Simon, Appleton, Louise, Farrah, Claire, Lau, Jonathan, Haroon, Nigil, Mulero, Juan, Blanco, Francisco J, Gonzalez-Gay, Miguel A, Lopez-Larrea, C, Bowness, Paul, Gaffney, Karl, Gaston, Hill, Gladman, Dafna D, Rahman, Proton, Maksymowych, Walter P, Crusius, J Bart A, van der Horst-Bruinsma, Irene E, Valle-Oñate, Raphael, Romero-Sánchez, Consuelo, Hansen, Inger Myrnes, Pimentel-Santos, Fernando M, Inman, Robert D, Martin, Javier, Breban, Maxime, Wordsworth, Bryan Paul, Reveille, John D, Evans, David M, de Bakker, Paul IW, and Brown, Matthew A

Subjects
Humans, Spondylitis, Ankylosing, Genetic Predisposition to Disease, Aminopeptidases, HLA-B27 Antigen, Minor Histocompatibility Antigens, Case-Control Studies, Major Histocompatibility Complex, Epistasis, Genetic, Polymorphism, Single Nucleotide, HLA-B40 Antigen, Epistasis, Genetic, Polymorphism, Single Nucleotide, Spondylitis, Ankylosing
Abstract

Ankylosing spondylitis (AS) is a common, highly heritable, inflammatory arthritis for which HLA-B*27 is the major genetic risk factor, although its role in the aetiology of AS remains elusive. To better understand the genetic basis of the MHC susceptibility loci, we genotyped 7,264 MHC SNPs in 22,647 AS cases and controls of European descent. We impute SNPs, classical HLA alleles and amino-acid residues within HLA proteins, and tested these for association to AS status. Here we show that in addition to effects due to HLA-B*27 alleles, several other HLA-B alleles also affect susceptibility. After controlling for the associated haplotypes in HLA-B, we observe independent associations with variants in the HLA-A, HLA-DPB1 and HLA-DRB1 loci. We also demonstrate that the ERAP1 SNP rs30187 association is not restricted only to carriers of HLA-B*27 but also found in HLA-B*40:01 carriers independently of HLA-B*27 genotype.

Published
2015

2. Major histocompatibility complex associations of ankylosing spondylitis are complex and involve further epistasis with ERAP1

Author

Cortes, Adrian, Pulit, Sara L, Leo, Paul J, Pointon, Jenny J, Robinson, Philip C, Weisman, Michael H, Ward, Michael, Gensler, Lianne S, Zhou, Xiaodong, Garchon, Henri-Jean, Chiocchia, Gilles, Nossent, Johannes, Lie, Benedicte A, Førre, Øystein, Tuomilehto, Jaakko, Laiho, Kari, Bradbury, Linda A, Elewaut, Dirk, Burgos-Vargas, Ruben, Stebbings, Simon, Appleton, Louise, Farrah, Claire, Lau, Jonathan, Haroon, Nigil, Mulero, Juan, Blanco, Francisco J, Gonzalez-Gay, Miguel A, Lopez-Larrea, C, Bowness, Paul, Gaffney, Karl, Gaston, Hill, Gladman, Dafna D, Rahman, Proton, Maksymowych, Walter P, Crusius, J Bart A, van der Horst-Bruinsma, Irene E, Valle-Oñate, Raphael, Romero-Sánchez, Consuelo, Hansen, Inger Myrnes, Pimentel-Santos, Fernando M, Inman, Robert D, Martin, Javier, Breban, Maxime, Wordsworth, Bryan Paul, Reveille, John D, Evans, David M, de Bakker, Paul IW, and Brown, Matthew A

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Autoimmune Disease, Clinical Research, Arthritis, 2.1 Biological and endogenous factors, Aetiology, Inflammatory and immune system, Aminopeptidases, Case-Control Studies, Epistasis, Genetic, Genetic Predisposition to Disease, HLA-B27 Antigen, HLA-B40 Antigen, Humans, Major Histocompatibility Complex, Minor Histocompatibility Antigens, Polymorphism, Single Nucleotide, Spondylitis, Ankylosing
Abstract

Ankylosing spondylitis (AS) is a common, highly heritable, inflammatory arthritis for which HLA-B*27 is the major genetic risk factor, although its role in the aetiology of AS remains elusive. To better understand the genetic basis of the MHC susceptibility loci, we genotyped 7,264 MHC SNPs in 22,647 AS cases and controls of European descent. We impute SNPs, classical HLA alleles and amino-acid residues within HLA proteins, and tested these for association to AS status. Here we show that in addition to effects due to HLA-B*27 alleles, several other HLA-B alleles also affect susceptibility. After controlling for the associated haplotypes in HLA-B, we observe independent associations with variants in the HLA-A, HLA-DPB1 and HLA-DRB1 loci. We also demonstrate that the ERAP1 SNP rs30187 association is not restricted only to carriers of HLA-B*27 but also found in HLA-B*40:01 carriers independently of HLA-B*27 genotype.

Published
2015

3. Farnesoid X receptor (FXR) activation and FXR genetic variation in inflammatory bowel disease.

Author

Nijmeijer, Rian M, Gadaleta, Raffaella M, van Mil, Saskia WC, van Bodegraven, Adriaan A, Crusius, J Bart A, Dijkstra, Gerard, Hommes, Daan W, de Jong, Dirk J, Stokkers, Pieter CF, Verspaget, Hein W, Weersma, Rinse K, van der Woude, C Janneke, Stapelbroek, Janneke M, Schipper, Marguerite EI, Wijmenga, Cisca, van Erpecum, Karel J, Oldenburg, Bas, and Dutch Initiative on Crohn, Colitis (ICC)

Subjects
Dutch Initiative on Crohn, Colitis, Colon, Ileum, Humans, Colitis, Ulcerative, Inflammatory Bowel Diseases, Receptors, Cytoplasmic and Nuclear, RNA, Messenger, Case-Control Studies, Gene Expression, Polymorphism, Single Nucleotide, Female, Male, Genetic Variation, General Science & Technology
Abstract

BackgroundWe previously showed that activation of the bile salt nuclear receptor Farnesoid X Receptor (FXR) protects against intestinal inflammation in mice. Reciprocally, these inflammatory mediators may decrease FXR activation. We investigated whether FXR activation is repressed in the ileum and colon of inflammatory bowel disease (IBD) patients in remission. Additionally, we evaluated whether genetic variation in FXR is associated with IBD.MethodsmRNA expression of FXR and FXR target gene SHP was determined in ileal and colonic biopsies of patients with Crohn's colitis (n = 15) and ulcerative colitis (UC; n = 12), all in clinical remission, and healthy controls (n = 17). Seven common tagging SNPs and two functional SNPs in FXR were genotyped in 2355 Dutch IBD patients (1162 Crohn's disease (CD) and 1193 UC) and in 853 healthy controls.ResultsmRNA expression of SHP in the ileum is reduced in patients with Crohn's colitis but not in patients with UC compared to controls. mRNA expression of villus marker Villin was correlated with FXR and SHP in healthy controls, a correlation that was weaker in UC patients and absent in CD patients. None of the SNPs was associated with IBD, UC or CD, nor with clinical subgroups of CD.ConclusionsFXR activation in the ileum is decreased in patients with Crohn's colitis. This may be secondary to altered enterohepatic circulation of bile salts or transrepression by inflammatory signals but does not seem to be caused by the studied SNPs in FXR. Increasing FXR activity by synthetic FXR agonists may have benefit in CD patients.

Published
2011

4. Farnesoid X Receptor (FXR) Activation and FXR Genetic Variation in Inflammatory Bowel Disease

Author

Nijmeijer, Rian M, Gadaleta, Raffaella M, van Mil, Saskia WC, van Bodegraven, Adriaan A, Crusius, J Bart A, Dijkstra, Gerard, Hommes, Daan W, de Jong, Dirk J, Stokkers, Pieter CF, Verspaget, Hein W, Weersma, Rinse K, van der Woude, C Janneke, Stapelbroek, Janneke M, Schipper, Marguerite EI, Wijmenga, Cisca, van Erpecum, Karel J, and Oldenburg, Bas

Subjects
Clinical Research, Digestive Diseases, Autoimmune Disease, Genetics, Crohn's Disease, Inflammatory Bowel Disease, 2.1 Biological and endogenous factors, Aetiology, Oral and gastrointestinal, Case-Control Studies, Colitis, Ulcerative, Colon, Female, Gene Expression, Genetic Variation, Humans, Ileum, Inflammatory Bowel Diseases, Male, Polymorphism, Single Nucleotide, RNA, Messenger, Receptors, Cytoplasmic and Nuclear, Dutch Initiative on Crohn, Colitis, General Science & Technology
Abstract

BackgroundWe previously showed that activation of the bile salt nuclear receptor Farnesoid X Receptor (FXR) protects against intestinal inflammation in mice. Reciprocally, these inflammatory mediators may decrease FXR activation. We investigated whether FXR activation is repressed in the ileum and colon of inflammatory bowel disease (IBD) patients in remission. Additionally, we evaluated whether genetic variation in FXR is associated with IBD.MethodsmRNA expression of FXR and FXR target gene SHP was determined in ileal and colonic biopsies of patients with Crohn's colitis (n = 15) and ulcerative colitis (UC; n = 12), all in clinical remission, and healthy controls (n = 17). Seven common tagging SNPs and two functional SNPs in FXR were genotyped in 2355 Dutch IBD patients (1162 Crohn's disease (CD) and 1193 UC) and in 853 healthy controls.ResultsmRNA expression of SHP in the ileum is reduced in patients with Crohn's colitis but not in patients with UC compared to controls. mRNA expression of villus marker Villin was correlated with FXR and SHP in healthy controls, a correlation that was weaker in UC patients and absent in CD patients. None of the SNPs was associated with IBD, UC or CD, nor with clinical subgroups of CD.ConclusionsFXR activation in the ileum is decreased in patients with Crohn's colitis. This may be secondary to altered enterohepatic circulation of bile salts or transrepression by inflammatory signals but does not seem to be caused by the studied SNPs in FXR. Increasing FXR activity by synthetic FXR agonists may have benefit in CD patients.

Published
2011

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