Correlation of genetic risk and messenger RNA expression in a Th17/IL23 pathway analysis in inflammatory bowel disease

Inflammatory Bowel Diseases

Volumn 20, Issue 5, 2014, Pages 777-782

  Fransen, Karin ^a   Van Sommeren, Suzanne ^a   Westra, Harm Jan ^a   Veenstra, Monique ^a   Lamberts, Letitia E ^a   Modderman, Rutger ^a   Dijkstra, Gerard ^a   Fu, Jingyuan ^a   Wijmenga, Cisca ^a   Franke, Lude ^a   Weersma, Rinse K ^a   Van Diemen, Cleo C ^a  

^a UNIVERSITY MEDICAL CENTER GRONINGEN   (Netherlands)

Author keywords

Genetic risk load; Inflammatory bowel disease; MRNA expression; Th17 IL23 pathway

Indexed keywords

CHEMOKINE RECEPTOR CCR6; IMMUNOMODULATING AGENT; INTERLEUKIN 23; INTERLEUKIN 23P19; MESALAZINE; MESSENGER RNA; RETINOID RELATED ORPHAN RECEPTOR GAMMA; STAT3 PROTEIN; INTERLEUKIN 17;

ADULT; ARTICLE; CLINICAL ASSESSMENT; COHORT ANALYSIS; CONTROLLED STUDY; CROHN DISEASE; FEMALE; GENE EXPRESSION; GENE FUNCTION; GENETIC ASSOCIATION; GENETIC RISK; GENOME; GENOTYPE; HUMAN; HUMAN CELL; IMMUNOPATHOLOGY; INFLAMMATORY BOWEL DISEASE; MAJOR CLINICAL STUDY; MALE; MIDDLE AGED; PERIPHERAL BLOOD MONONUCLEAR CELL; POLYMERASE CHAIN REACTION; PRIORITY JOURNAL; QUANTITATIVE ANALYSIS; QUANTITATIVE TRAIT LOCUS; SIGNAL TRANSDUCTION; SINGLE NUCLEOTIDE POLYMORPHISM; TH17 CELL; ULCERATIVE COLITIS; CYTOLOGY; GENETICS; METABOLISM; MONONUCLEAR CELL; PATHOLOGY; PROGNOSIS; RISK FACTOR;

COLITIS, ULCERATIVE; CROHN DISEASE; FEMALE; GENOTYPE; HUMANS; INTERLEUKIN-17; INTERLEUKIN-23; LEUKOCYTES, MONONUCLEAR; MALE; MIDDLE AGED; PROGNOSIS; QUANTITATIVE TRAIT LOCI; RISK FACTORS; RNA, MESSENGER; SIGNAL TRANSDUCTION; TH17 CELLS;

EID: 84902181350     PISSN: 10780998     EISSN: 15364844     Source Type: Journal    
DOI: 10.1097/MIB.0000000000000013     Document Type: Article

References (24)

1. Nell S, Suerbaum S, Josenhans C. The impact of the microbiota on the pathogenesis of IBD: lessons from mouse infection models. Nat Rev Microbiol. 2010;8:564-577.
2. Molodecky NA, Soon IS, Rabi DM, et al. Increasing incidence and prevalence of the inflammatory bowel diseases with time, based on systematic review. Gastroenterology. 2012;142:46-54.
3. Jostins L, Ripke S, Weersma RK, et al. Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease. Nature. 2012;491:119-124.
4. Rossin EJ, Lage K, Raychaudhuri S, et al. Proteins encoded in genomic regions associated with immune-mediated disease physically interact and suggest underlying biology. PLoS Genet. 2011;7:e1001273.
5. Raychaudhuri S, Plenge RM, Rossin EJ, et al. Identifying relationships among genomics disease regions: predicting genes at pathogenic SNP associations and rare deletions. PLoS Genet. 2009;5:e1000534.
6. Abraham C, Cho J. Interleukin-23/Th17 pathways and inflammatory bowel disease. In flamm Bowel Dis. 2009;15:1090-1100.
7. Pidasheva S, Trifari S, Phillips A, et al. Functional studies on the IBD susceptibility gene IL23R implicate reduced receptor function in the protective genetic variant R381Q. PLoS One. 2011;6:e25038.
8. Olsen T, Rismo R, Cui G, et al. TH1 and TH17 interactions in untreated inflamed mucosa of inflammatory bowel disease, and their potential to mediate the inflammation. Cytokine. 2011;56:633-640.
9. Bogaert S, Laukens D, Peeters H, et al. Differential mucosal expression of Th17-related genes between the inflamed colon and ileum of patients with inflammatory bowel disease. BMC Immunol. 2010;11:61.
10. Sugihara T, Kobori A, Imaeda H, et al. The increased mucosal mRNA expressions of complement C3 and interleukin-17 in inflammatory bowel disease. Clin Exp Immunol. 2010;160:386-393.
11. Kobayashi T, Okamoto S, Hisamatsu T, et al. IL23 differentially regulates the Th1/Th17 balance in ulcerative colitis and Crohn's disease. Gut. 2008; 57:1682-1689.
12. Dige A, Støy S, Rasmussen TK, et al. Increased levels of circulating Th17 cells in quiescent versus active Crohn's disease. J Crohns Colitis. 2013;7: 248-255.
13. Nicolae DL, Gamazon E, Zhang W, et al. Trait-associated SNPs are more likely to be eQTLs: annotation to enhance discovery from GWAS. PLoS Genet. 2010;6:e1000888.
14. Schadt EE, Lamb J, Yang X, et al. An integrative genomics approach to infer causal associations between gene expression and disease. Nat Genet. 2005;37:710-717.
15. Emilsson V, Thorleifsson G, Zhang B, et al. Genetics of gene expression and its effect on disease. Nature. 2008;452:423-428.
16. Naukkarinen J, Surakka I, Pietilainen KH, et al. Use of genome-wide expression data to Mine the "Gray Zone" of GWA studies leads to novel candidate obesity genes. PLoS Genet. 2010;6:e1000976.
17. Podolsky DK. Inflammatory bowel disease. N Engl J Med. 2002;347: 417-429.
18. Hölttä V, Sipponen T, Westerholm-Ormio M, et al. In Crohn's disease, anti-TNF-a treatment changes the balance between mucosal IL-17, FOXP3, and CD4 cells. ISRN Gastroenterol. 2012;2012:505432.
19. Fehrmann RS, Jansen RC, Veldink JH, et al. Trans-eQTLs reveal that independent genetic variants associated with a complex phenotype converge on intermediate genes, with a major role for the HLA. PLoS Genet. 2011;7:e1002197.
20. Fu J, Wolfs MG, Deelen P, et al. Unraveling the regulatory mechanisms underlying tissue-dependent genetic variation of gene expression. PLoS Genet. 2012;8:e1002431.
21. Rivas MA, Beaudoin M, Gardet A, et al. Deep resequencing of GWAS loci identifies independent rare variants associated with inflammatory bowel disease. Nat Genet. 2011;43:1066-1073.
22. Hunt KA, Mistry V, Bockett NA, et al. Negligible impact of rare autoimmune-locus coding-region variants on missing heritability. Nature. 2013;498:232-235.
23. Mao H, Yang W, Lee PP, et al. Exome sequencing identifies novel compound heterozygous mutations of IL-10 receptor 1 in neonatal-onset Crohn's disease. Genes Immun. 2012;13:437-442.
24. The ENCODE Project Consortium. An integrated encyclopedia of DNA elements in the human genome. Nature. 2012;489:57-74.