scholarly journals Interleukin-23/Th17 pathways and inflammatory bowel disease

2009 ◽  
Vol 15 (7) ◽  
pp. 1090-1100 ◽  
Author(s):  
Clara Abraham ◽  
Judy Cho
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Inflammatory Bowel ◽  
Interleukin 23

scholarly journals Replication of interleukin 23 receptor and autophagyrelated 16-like 1 association in adult- and pediatric-onset inflammatory bowel disease in Italy

2008 ◽  
Vol 14 (29) ◽  
pp. 4643 ◽  
Author(s):  
Anna Latiano ◽  
Orazio Palmieri ◽  
Maria Rosa Valvano ◽  
Renata D’Incà ◽  
Salvatore Cucchiara ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Inflammatory Bowel ◽  
Interleukin 23 ◽  
Pediatric Onset

scholarly journals Psoriasis and Inflammatory Bowel Disease

2019 ◽  
Vol 37 (6) ◽  
pp. 451-457 ◽  
Author(s):  
Mario Cottone ◽  
Chiara Sapienza ◽  
Fabio Salvatore Macaluso ◽  
Marco Cannizzaro
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Immunological Mechanisms ◽  
Predisposition Genes ◽  
Associated Conditions ◽  
Inflammatory Bowel ◽  
Interleukin 23 ◽  
Risk Of Cancer ◽  
Similar Risk ◽  
Necrosis Factor

Background: Inflammatory bowel disease (IBD) and psoriasis (PS) are associated conditions. The reason for this association lies in the sharing of predisposition genes and common immunological mechanisms. Summary: This review will focus on the interplay between IBD and PS, with details on prevalence and phenotype of PS in IBD, genetics, pathogenetic pathways, and therapy. Key Messages: Microbiome seems relevant in both conditions: a reduction of beneficial bacteria has been observed. IBD and PS have in common some comorbidities like cardiovascular disease, similar risk of cancer and psychiatric problems. Many biological therapies such as anti-tumour necrosis factor (TNF) and anti-interleukin 23 are effective in both conditions, underlining the common immunological mechanisms. Paradoxical PS has been mainly observed after anti-TNF therapies, but preliminary reports show that it can also occur with other biologics. Genetic predisposition to this phenomenon has been reported.

CO9 ROLE OF INTERLEUKIN-23 RECEPTOR IN PEDIATRIC-ONSET INFLAMMATORY BOWEL DISEASE AND GENOTYPE-PHENOTYPE ASSOCIATION

2010 ◽  
Vol 42 ◽  
pp. S325
Author(s):  
L. Quaglietta ◽  
A.A. te Velde ◽  
C. Friano ◽  
S. Meisner ◽  
E. Miele ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Inflammatory Bowel ◽  
Interleukin 23 ◽  
Pediatric Onset

After interleukin-12p40, are interleukin-23 and interleukin-17 the next therapeutic targets for inflammatory bowel disease?

2007 ◽  
Vol 7 (4) ◽  
pp. 409-416 ◽  
Author(s):  
Zili Zhang ◽  
David J. Hinrichs ◽  
Huiying Lu ◽  
Hong Chen ◽  
Wenwei Zhong ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Therapeutic Targets ◽  
Interleukin 17 ◽  
Inflammatory Bowel ◽  
Interleukin 23

scholarly journals Replication and Meta-Analysis of 13,000 Cases Defines the Risk for Interleukin-23 Receptor and Autophagy-Related 16-Like 1 Variants in Crohn’s Disease

2010 ◽  
Vol 24 (5) ◽  
pp. 297-302 ◽  
Author(s):  
Lynn Cotterill ◽  
Debbie Payne ◽  
Scott Levison ◽  
John McLaughlin ◽  
Emma Wesley ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Bowel Disease ◽  
Meta Analysis ◽  
European Ancestry ◽  
Published Data ◽  
Increased Risk ◽  
Inflammatory Bowel ◽  
Interleukin 23

BACKGROUND/OBJECTIVE: Variants in the interleukin-23 receptor (IL23R) and the autophagy-related 16-like 1 (ATG16L1) genes have been associated with an increased risk of Crohn’s disease (CD). Both genes were identified through genome-wide association scans and subsequent studies have validated these associations. To assess the effect size of these variants, an independent case-control association study and meta-analysis were performed.METHODS: British Caucasian subjects with inflammatory bowel disease (n=500) and 877 ethnically matched controls were genotyped for the disease-associated variants inIL23RandATG16L1. In addition, meta-analyses of 12,991 patients and 14,598 controls, and 11,909 patients and 15,798 controls, were conducted on independently published data for the associations betweenIL23RandATG16L1variants and CD, respectively.RESULTS: In the present cohort, both susceptibility variants showed highly significant associations, includingIL23R(rs11209026, P=0.0006; OR 0.37; 95% CI 0.21 to 0.67) andATG16L1(rs2241880, P=0.0017; OR 1.36; 95% CI 1.12 to 1.66). The meta-analysis based on the random effects model showed similar combined effects for rs11209026 (n=26, OR 0.41; 95% CI 0.37 to 0.46) and rs2241880 (n=25, OR 1.33; 95% CI 1.28 to 1.39). There was no statistically significant gene-gene interaction between caspase recruitment domain (CARD15) variants and theIL23RorATG16L1polymorphisms (P=0.44 and P=0.24, respectively).CONCLUSION: The present cohort and meta-analysis provides strong evidence that, in addition toCARD15, polymorphisms in bothIL23RandATG16L1alter susceptibility to CD and that these effects are consistent across all populations of European ancestry; however, onlyATG16L1is relevant to inflammatory bowel disease in the Asian population.

scholarly journals Genetic Studies of Inflammatory Bowel Disease-Focusing on Asian Patients

Cells ◽  
2019 ◽  
Vol 8 (5) ◽  
pp. 404 ◽  
Author(s):  
Sung Chul Park ◽  
Yoon Tae Jeen
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Genetic Variants ◽  
Intestinal Inflammation ◽  
Human Leukocyte ◽  
Risk Modeling ◽  
Genetic Studies ◽  
Asian Patients ◽  
Inflammatory Bowel ◽  
Interleukin 23

The pathogenesis of inflammatory bowel disease (IBD) is not well-understood; however, increased and persistent intestinal inflammation, due to inappropriate immune responses that are caused by interactions between genetic factors, gut microbiota, and environmental factors, are thought to lead to IBD. Various studies have identified more than 240 genetic variants related to IBD. These genetic variants are involved in innate and adaptive immunity, autophagy, defective bacterial handing, interleukin-23 and 10 signaling, and so on. According to several epidemiological and clinical studies, the phenotypes and clinical course of IBD differ between Asians and Europeans. Although the risk loci for IBD typically overlap between Asians and Westerners, genetic heterogeneity has been detected in many loci/genes, such as NOD2/CARD15, TNFSF15 and human leukocyte antigen, contributing to the risk of IBD. Thus, although common pathways exist between Westerners and Asians in the development of IBD, their significance may differ for individual pathways. Although genetic studies are not universally applicable in the clinical field, they may be useful for diagnosing and categorizing IBD, predicting therapeutic responses and toxicity to drugs, and assessing prognosis by risk modeling, thereby enabling precision medicine for individual patients.

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