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Recent Insights Into the Genetics of Inflammatory Bowel Disease
Open accessAbstract
Inflammatory bowel diseases (IBDs) are complex, multifactorial disorders that comprise Crohn's disease (CD) and ulcerative colitis (UC). Genome-wide association studies have identified approximately 100 loci that are significantly associated with IBD. These loci implicate a diverse array of genes and pathophysiologic mechanisms, including microbe recognition, lymphocyte activation, cytokine signaling, and intestinal epithelial defense. Consistent with epidemio-logic predictions, many IBD-associated loci demonstrate genome-wide significant associations to both CD and UC, notably, genes whose products function in the interleukin-23 pathway, and transcription factors, including NK2 transcription factor related, locus 3 (NKX2-3), SMAD3, STAT3, ZMIZ1, and c-REL. Although CD and UC are both associated with genomic regions that implicate products of genes involved in leukocyte trafficking, there is evidence for association patterns that are distinct between CD and UC. CD-predominant associations include NOD2 and genes that regulate autophagy. In UC, the predominant association signal is on chromosome 6p21, in the major histocompatibility complex region, near HLA class II genes. UC-predominant loci have also implicated genes mediating epithelial defense function. There is a striking overlap of loci between diseases, which could provide comparative insight into mechanisms of disease pathogenesis. Genes that encode factors that function in the interleukin-23 pathway have been associated with a number of chronic inflammatory diseases, notably psoriasis and anky-losing spondylitis. Distinct genetic associations indicate that the colitis associated with primary sclerosing cholangitis is pathophysiologically distinct from UC that is not associated with primary sclerosing cholangitis. As many as 14 susceptibility loci are shared between IBD and celiac disease, indicating significant overlap in pathophysiology. Future genetic studies will be directed toward identifying un common variations with potentially greater statistical effects, defining population differences, and more completely accounting for familial transmission of disease.
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Cites
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Genome-wide association defines more than 30 distinct susceptibility loci for Crohn's disease
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Cited by
Rogler, G., Singh, A., Kavanaugh, A., & Rubin, D. T. (2021) · Gastroenterology · doi:10.1053/j.gastro.2021.07.042 · Cited by 869
Chassaing, B., Srinivasan, G., Delgado, M. A., Young, A. N., Gewirtz, A. T., & Vijay-Kumar, M. (2012) · PLoS ONE · doi:10.1371/journal.pone.0044328 · Cited by 554
Carvalho, F. A., Koren, O., Goodrich, J. K., Johansson, M. E. V., Nalbantoglu, I., Aitken, J. D., Su, Y., Chassaing, B., Walters, W. A., González, A., et al. (2012) · Cell Host & Microbe · doi:10.1016/j.chom.2012.07.004 · Cited by 548
Interactions between Intestinal Microbiota and Host Immune Response in Inflammatory Bowel Disease
Zhang, M., Sun, K., Wu, Y., Yang, Y., Tso, P., & Wu, Z. (2017) · Frontiers in Immunology · doi:10.3389/fimmu.2017.00942 · Cited by 347
Dysbiosis in Inflammatory Bowel Disease: Pathogenic Role and Potential Therapeutic Targets
Santana, P. T., Rosas, S. L. B., Ribeiro, B. E., Marinho, Y., & de Souza, H. S. P. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23073464 · Cited by 325
Metadata
- Authors
- Cho, J. H., & Brant, S. R.
- Venue
- Gastroenterology
- Publisher
- Elsevier BV
- Published
- 2011-05
- Volume
- 140
- Issue
- 6
- Pages
- 1704-1712.e2
- ISSN
- 0016-5085 (ISSN-L)
- OpenAlex
- W1983251816
- Cited by
- 425
- References
- 100
- FWCI
- 29.42
- Type
- journal article
- Language
- en
- Open access
- bronze
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