Polymorphism in the interleukin (IL-10) gene in patients with inflammatory bowel disease

Aithal, P.G.; Grove, Jane I.; Daly, AK; Han, S; Welfare, Mark; Jones, DE; Day, CP; Hudson, M

doi:10.1016/s0016-5085(98)83739-6

Cited by 2 publications

(2 citation statements)

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“…Some studies demonstrated association between variant polymorphisms of metabolic enzymes and IBD: methylenetetrahydrofolate reductase C677T [53], glutathione S-transferases GSTM1 and GSTT1 [54], peroxisome proliferators-activated receptors [55], multidrug resistance 1 gene [56], IL-10 [57], keratin 8 [58], IL-4 [59], hMLH1 mismatch repair gene [60], IL-11 gene [61], TNF-α 308 [62], NF-κB1 promoter [63], p53 [64], CD14 [65], and BsmI vitamin D receptor gene in Ashkenazi Jews [66]. Whether polymorphisms in any of these genes have an influence on IBD, or serve merely as markers in LD with susceptibility genes, remains unclear.…”

Section: Bacterial Recognition Oligomerizationmentioning

confidence: 99%

“…Other mechanistic molecular models, such as epigenetics, may also play a role in the initiation and progression of IBD and should be explored [19]. Genomic approaches employing SNPs could facilitate the study of polymorphic variants that influence IBD or serve as markers in linkage studies [53][54][55][56][57][58][59][60][61][62][63][64][65][66]. Transcriptomic approaches could facilitate the identification of disease subgroups on the basis of gene expression signatures, and could predict disease behavior or optimal response to therapy [67][68][69][70].…”

Section: Decreased Induction/secretion Of Gstsmentioning

confidence: 99%

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Role of genes, the environment and their interactions in the etiology of inflammatory bowel diseases

Ahmed¹

2006

Expert Review of Molecular Diagnostics

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Few of the studied genes demonstrate association with inflammatory bowel disease (IBD). Three mutations in the nucleotide-binding oligomerization domain 2 gene have consistently shown to be independent risk factors for Crohn's disease, but none of the alleles exhibited high sensitivity or specificity for IBD. Linkage analysis implicated several loci on various chromosomes, and epistasis has been demonstrated. The etiopathogenesis of IBD remains unknown, and environmental contribution to their pathogenesis is evident from genetic studies that demonstrated incomplete monozygotic twins concordandance rate for both Crohn's and ulcerative colitis. Smoking has shown an opposite effect on disease phenotype, with an adverse effect on disease course for Crohn's disease, but a slight beneficial effect in ulcerative colitis. The contribution of infectious agents to susceptibility to IBD appears to be strong. However, the role of nutrition on the etiology and therapy of IBD is not clear. Inconsistencies in environmental risk factors could be due to gene-environment interactions, making it essential to study the role of genetics and environmental contribution to the etiopathology of IBD. Transgenic or knockout mice, such as interleukin-10(-/-), T-cell receptor alpha(-/-), Galphai(2) (-/-) and N-cadherin(-/-), develop colitis-like inflammation similar to humans. Therefore, animal models must be further studied to explore mechanistic interactions.

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