Investigation of JAK2, STAT3 and CCR6 polymorphisms and their gene-gene interactions in inflammatory bowel disease
Summary Genome‐wide association studies identified many loci associated with the two forms of inflammatory bowel disease (IBD), Crohn’s disease (CD) and ulcerative colitis (UC). Components of the interleukin‐23 signalling pathway, such as IL23R, JAK2 and STAT3, have been implicated in both diseases....
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| Published in | International journal of immunogenetics Vol. 39; no. 3; pp. 247 - 252 |
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| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford, UK
Blackwell Publishing Ltd
01.06.2012
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Summary
Genome‐wide association studies identified many loci associated with the two forms of inflammatory bowel disease (IBD), Crohn’s disease (CD) and ulcerative colitis (UC). Components of the interleukin‐23 signalling pathway, such as IL23R, JAK2 and STAT3, have been implicated in both diseases. In addition, emerging evidence supports the role of IL23‐driven Th17 cells in inflammation. Here, we studied the susceptibility nature of three components of IL23 signalling and Th17 cell differentiation: JAK2 rs10758669, STAT3 rs744166 and CCR6 rs2301436 initially associated with CD in Hungarian CD and UC patients. A total of 616 unrelated subjects with either form of IBD and 496 healthy controls were genotyped with PCR‐RFLP methods. We also tested the genetic interactions of JAK2, STAT3 and CCR6 polymorphisms in a pairwise fashion with regard to disease risk. We could confirm the susceptibility of STAT3 rs744166 TT homozygotes for UC (OR: 1.483, 95% CI: 1.103–1.992, P = 0.009). Data on genetic interaction reveals that the above JAK2 and STAT3 risk alleles contribute to CD susceptibility in combination with each other (OR: 2.218; 95% CI: 1.097–4.487; P = 0.024), while the JAK2 variant shows a tendency to confer UC risk only on a wild‐type STAT3 background (OR: 1.997, 95%CI: 0.994–4.009, P = 0.049). Our results may help in understanding how these natural variants contribute to development of IBD through their genetic association. |
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| AbstractList | Summary
Genome‐wide association studies identified many loci associated with the two forms of inflammatory bowel disease (IBD), Crohn’s disease (CD) and ulcerative colitis (UC). Components of the interleukin‐23 signalling pathway, such as IL23R, JAK2 and STAT3, have been implicated in both diseases. In addition, emerging evidence supports the role of IL23‐driven Th17 cells in inflammation. Here, we studied the susceptibility nature of three components of IL23 signalling and Th17 cell differentiation: JAK2 rs10758669, STAT3 rs744166 and CCR6 rs2301436 initially associated with CD in Hungarian CD and UC patients. A total of 616 unrelated subjects with either form of IBD and 496 healthy controls were genotyped with PCR‐RFLP methods. We also tested the genetic interactions of JAK2, STAT3 and CCR6 polymorphisms in a pairwise fashion with regard to disease risk. We could confirm the susceptibility of STAT3 rs744166 TT homozygotes for UC (OR: 1.483, 95% CI: 1.103–1.992, P = 0.009). Data on genetic interaction reveals that the above JAK2 and STAT3 risk alleles contribute to CD susceptibility in combination with each other (OR: 2.218; 95% CI: 1.097–4.487; P = 0.024), while the JAK2 variant shows a tendency to confer UC risk only on a wild‐type STAT3 background (OR: 1.997, 95%CI: 0.994–4.009, P = 0.049). Our results may help in understanding how these natural variants contribute to development of IBD through their genetic association. Genome-wide association studies identified many loci associated with the two forms of inflammatory bowel disease (IBD), Crohn's disease (CD) and ulcerative colitis (UC). Components of the interleukin-23 signalling pathway, such as IL23R, JAK2 and STAT3, have been implicated in both diseases. In addition, emerging evidence supports the role of IL23-driven Th17 cells in inflammation. Here, we studied the susceptibility nature of three components of IL23 signalling and Th17 cell differentiation: JAK2 rs10758669, STAT3 rs744166 and CCR6 rs2301436 initially associated with CD in Hungarian CD and UC patients. A total of 616 unrelated subjects with either form of IBD and 496 healthy controls were genotyped with PCR-RFLP methods. We also tested the genetic interactions of JAK2, STAT3 and CCR6 polymorphisms in a pairwise fashion with regard to disease risk. We could confirm the susceptibility of STAT3 rs744166 TT homozygotes for UC (OR: 1.483, 95% CI: 1.103-1.992, P = 0.009). Data on genetic interaction reveals that the above JAK2 and STAT3 risk alleles contribute to CD susceptibility in combination with each other (OR: 2.218; 95% CI: 1.097-4.487; P = 0.024), while the JAK2 variant shows a tendency to confer UC risk only on a wild-type STAT3 background (OR: 1.997, 95%CI: 0.994-4.009, P = 0.049). Our results may help in understanding how these natural variants contribute to development of IBD through their genetic association.Genome-wide association studies identified many loci associated with the two forms of inflammatory bowel disease (IBD), Crohn's disease (CD) and ulcerative colitis (UC). Components of the interleukin-23 signalling pathway, such as IL23R, JAK2 and STAT3, have been implicated in both diseases. In addition, emerging evidence supports the role of IL23-driven Th17 cells in inflammation. Here, we studied the susceptibility nature of three components of IL23 signalling and Th17 cell differentiation: JAK2 rs10758669, STAT3 rs744166 and CCR6 rs2301436 initially associated with CD in Hungarian CD and UC patients. A total of 616 unrelated subjects with either form of IBD and 496 healthy controls were genotyped with PCR-RFLP methods. We also tested the genetic interactions of JAK2, STAT3 and CCR6 polymorphisms in a pairwise fashion with regard to disease risk. We could confirm the susceptibility of STAT3 rs744166 TT homozygotes for UC (OR: 1.483, 95% CI: 1.103-1.992, P = 0.009). Data on genetic interaction reveals that the above JAK2 and STAT3 risk alleles contribute to CD susceptibility in combination with each other (OR: 2.218; 95% CI: 1.097-4.487; P = 0.024), while the JAK2 variant shows a tendency to confer UC risk only on a wild-type STAT3 background (OR: 1.997, 95%CI: 0.994-4.009, P = 0.049). Our results may help in understanding how these natural variants contribute to development of IBD through their genetic association. Genome‐wide association studies identified many loci associated with the two forms of inflammatory bowel disease (IBD), Crohn’s disease (CD) and ulcerative colitis (UC). Components of the interleukin‐23 signalling pathway, such as IL23R , JAK2 and STAT3, have been implicated in both diseases. In addition, emerging evidence supports the role of IL23‐driven Th17 cells in inflammation. Here, we studied the susceptibility nature of three components of IL23 signalling and Th17 cell differentiation: JAK2 rs10758669, STAT3 rs744166 and CCR6 rs2301436 initially associated with CD in Hungarian CD and UC patients. A total of 616 unrelated subjects with either form of IBD and 496 healthy controls were genotyped with PCR‐RFLP methods. We also tested the genetic interactions of JAK2, STAT3 and CCR6 polymorphisms in a pairwise fashion with regard to disease risk. We could confirm the susceptibility of STAT3 rs744166 TT homozygotes for UC (OR: 1.483, 95% CI: 1.103–1.992, P = 0.009). Data on genetic interaction reveals that the above JAK2 and STAT3 risk alleles contribute to CD susceptibility in combination with each other (OR: 2.218; 95% CI: 1.097–4.487; P = 0.024), while the JAK2 variant shows a tendency to confer UC risk only on a wild‐type STAT3 background (OR: 1.997, 95%CI: 0.994–4.009, P = 0.049). Our results may help in understanding how these natural variants contribute to development of IBD through their genetic association. Genome-wide association studies identified many loci associated with the two forms of inflammatory bowel disease (IBD), Crohn's disease (CD) and ulcerative colitis (UC). Components of the interleukin-23 signalling pathway, such as IL23R, JAK2 and STAT3, have been implicated in both diseases. In addition, emerging evidence supports the role of IL23-driven Th17 cells in inflammation. Here, we studied the susceptibility nature of three components of IL23 signalling and Th17 cell differentiation: JAK2 rs10758669, STAT3 rs744166 and CCR6 rs2301436 initially associated with CD in Hungarian CD and UC patients. A total of 616 unrelated subjects with either form of IBD and 496 healthy controls were genotyped with PCR-RFLP methods. We also tested the genetic interactions of JAK2, STAT3 and CCR6 polymorphisms in a pairwise fashion with regard to disease risk. We could confirm the susceptibility of STAT3 rs744166 TT homozygotes for UC (OR: 1.483, 95% CI: 1.103-1.992, P = 0.009). Data on genetic interaction reveals that the above JAK2 and STAT3 risk alleles contribute to CD susceptibility in combination with each other (OR: 2.218; 95% CI: 1.097-4.487; P = 0.024), while the JAK2 variant shows a tendency to confer UC risk only on a wild-type STAT3 background (OR: 1.997, 95%CI: 0.994-4.009, P = 0.049). Our results may help in understanding how these natural variants contribute to development of IBD through their genetic association. |
| Author | Csongei, V. Tulassay, Z. Melegh, B. I. Sumegi, K. Nagy, G. Szabo, M. Zambo, V. Polgar, N. Melegh, B. |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/22269120$$D View this record in MEDLINE/PubMed |
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A study of heritability and the influence of smoking publication-title: Gut – volume: 448 start-page: 427 year: 2007 article-title: Unravelling the pathogenesis of inflammatory bowel disease publication-title: Nature – volume: 40 start-page: 713 year: 2008 article-title: Replication of signals from recent studies of crohn’s disease identifies previously unknown disease loci for ulcerative colitis publication-title: Nature Genetics – volume: 29 start-page: 815 year: 2009 article-title: Strong evidence of a combination polymorphism of the tyrosine kinase 2 gene and the signal transducer and activator of transcription 3 gene as a dna‐based biomarker for susceptibility to crohn’s disease in the japanese population publication-title: Journal of Clinical Immunology – volume: 16 start-page: 176 year: 2010 article-title: Interaction of the major inflammatory bowel disease susceptibility alleles in crohn’s disease patients publication-title: World Journal of Gastroenterology – volume: 43 start-page: 246 year: 2011 article-title: Meta‐analysis identifies 29 additional ulcerative colitis risk loci, increasing the number of confirmed associations to 47 publication-title: Nature Genetics – volume: 40 start-page: 710 year: 2008 article-title: Genetic determinants of ulcerative colitis include the ecm1 locus and five loci implicated in crohn’s disease publication-title: Nature Genetics – ident: e_1_2_6_6_1 doi: 10.1136/gut.2008.163667 – ident: e_1_2_6_26_1 doi: 10.1038/ajg.2009.184 – ident: e_1_2_6_10_1 doi: 10.1038/ng.145 – ident: e_1_2_6_12_1 doi: 10.1038/ng.717 – ident: e_1_2_6_8_1 doi: 10.1126/science.1135245 – ident: e_1_2_6_29_1 doi: 10.1002/1521-4141(200201)32:1<231::AID-IMMU231>3.0.CO;2-8 – ident: e_1_2_6_15_1 doi: 10.1038/ng1954 – ident: e_1_2_6_16_1 doi: 10.1038/ng.489 – ident: e_1_2_6_21_1 doi: 10.1159/000073735 – ident: e_1_2_6_25_1 doi: 10.1007/s10875-009-9320-x – ident: e_1_2_6_2_1 doi: 10.1038/ajg.2009.179 – ident: e_1_2_6_24_1 doi: 10.1038/ng2032 – ident: e_1_2_6_13_1 doi: 10.1038/ajg.2009.163 – ident: e_1_2_6_30_1 doi: 10.1038/nature06005 – ident: e_1_2_6_28_1 doi: 10.1136/gut.29.7.990 – ident: e_1_2_6_23_1 doi: 10.1371/journal.pone.0005472 – ident: e_1_2_6_14_1 doi: 10.1002/ibd.21295 – ident: e_1_2_6_31_1 doi: 10.1074/jbc.C600321200 – ident: e_1_2_6_18_1 doi: 10.1093/hmg/ddh079 – ident: e_1_2_6_3_1 doi: 10.1053/j.gastro.2008.10.032 – ident: e_1_2_6_9_1 doi: 10.1016/j.mrfmmm.2010.01.017 – ident: e_1_2_6_20_1 doi: 10.3109/00365529109025046 – ident: e_1_2_6_22_1 doi: 10.1038/ng0105-13 – ident: e_1_2_6_7_1 doi: 10.3748/wjg.v16.i2.176 – ident: e_1_2_6_27_1 doi: 10.1053/j.gastro.2007.02.051 – ident: e_1_2_6_5_1 doi: 10.1038/ng.175 – ident: e_1_2_6_11_1 doi: 10.1038/ng.148 – ident: e_1_2_6_19_1 doi: 10.1136/gut.2006.115402 – ident: e_1_2_6_17_1 doi: 10.1136/gut.2009.199679 – ident: e_1_2_6_4_1 doi: 10.1038/ng.764 |
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Genome‐wide association studies identified many loci associated with the two forms of inflammatory bowel disease (IBD), Crohn’s disease (CD) and... Genome‐wide association studies identified many loci associated with the two forms of inflammatory bowel disease (IBD), Crohn’s disease (CD) and ulcerative... Genome-wide association studies identified many loci associated with the two forms of inflammatory bowel disease (IBD), Crohn's disease (CD) and ulcerative... |
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| SubjectTerms | Adult Colitis, Ulcerative - genetics Crohn Disease - genetics Epistasis, Genetic Female Gene Frequency Genetic Predisposition to Disease - genetics Genotype Humans Hungary Inflammatory Bowel Diseases - genetics Janus Kinase 2 - genetics Logistic Models Male Middle Aged Polymerase Chain Reaction Polymorphism, Restriction Fragment Length Polymorphism, Single Nucleotide Receptors, CCR6 - genetics STAT3 Transcription Factor - genetics |
| Title | Investigation of JAK2, STAT3 and CCR6 polymorphisms and their gene-gene interactions in inflammatory bowel disease |
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