{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["14"],"submitter":["Cai Y"],"pubmed_abstract":["<h4>Introduction</h4>Observational studies have discovered a contradictory phenomenon between interleukin-17 (IL-17) and inflammatory bowel disease (IBD). The study aimed to confirm the causal association between each subtype of IL-17 and IBD.<h4>Methods</h4>We performed a 2-sample univariable and multivariable mendelian randomization (MR) to determine which subtype of IL-17 is causally related to IBD and its subtypes, and used a series of sensitivity analysis to examine the reliability of the main MR assumptions.<h4>Results</h4>We found that IL-17B, IL-17E and IL-17RB were significantly associated with an increased risk of UC (IL-17B: OR: 1.26, 95% CI, 1.09-1.46, P < 0.01; IL-17E: OR: 1.17, 95% CI, 1.05-1.30, P < 0.01; IL-17RB: OR: 1.30, 95% CI, 1.20-1.40, P < 0.0001) while IL-17C and IL-17RC showed causal effects on the increased risk of CD (IL-17C: OR: 1.23, 95% CI, 1.21-1.26, P < 0.0001; IL-17RC: OR: 2.01, 95% CI, 1.07-3.75, P=0.03). The results of multivariable MR (MVMR) showed that the causal effects of IL-17B and IL-17E on UC were unilaterally dependent on IL-17RB, while the effects of IL-17C and IL-17RC on CD were interdependent.<h4>Discussion</h4>Our study provided new genetic evidence for the causal relationships between each subtype of IL-17 and IBD, promoting future mechanistic research in IBD."],"journal":["Frontiers in immunology"],"pagination":["1238457"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10690942"],"repository":["biostudies-literature"],"pubmed_title":["Interleukin-17 and inflammatory bowel disease: a 2-sample Mendelian randomization study."],"pmcid":["PMC10690942"],"pubmed_authors":["Xu L","Cai J","Cai Y","Jia X","Chen H","Xie S"],"additional_accession":[]},"is_claimable":false,"name":"Interleukin-17 and inflammatory bowel disease: a 2-sample Mendelian randomization study.","description":"<h4>Introduction</h4>Observational studies have discovered a contradictory phenomenon between interleukin-17 (IL-17) and inflammatory bowel disease (IBD). The study aimed to confirm the causal association between each subtype of IL-17 and IBD.<h4>Methods</h4>We performed a 2-sample univariable and multivariable mendelian randomization (MR) to determine which subtype of IL-17 is causally related to IBD and its subtypes, and used a series of sensitivity analysis to examine the reliability of the main MR assumptions.<h4>Results</h4>We found that IL-17B, IL-17E and IL-17RB were significantly associated with an increased risk of UC (IL-17B: OR: 1.26, 95% CI, 1.09-1.46, P < 0.01; IL-17E: OR: 1.17, 95% CI, 1.05-1.30, P < 0.01; IL-17RB: OR: 1.30, 95% CI, 1.20-1.40, P < 0.0001) while IL-17C and IL-17RC showed causal effects on the increased risk of CD (IL-17C: OR: 1.23, 95% CI, 1.21-1.26, P < 0.0001; IL-17RC: OR: 2.01, 95% CI, 1.07-3.75, P=0.03). The results of multivariable MR (MVMR) showed that the causal effects of IL-17B and IL-17E on UC were unilaterally dependent on IL-17RB, while the effects of IL-17C and IL-17RC on CD were interdependent.<h4>Discussion</h4>Our study provided new genetic evidence for the causal relationships between each subtype of IL-17 and IBD, promoting future mechanistic research in IBD.","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023","modification":"2025-04-05T11:45:38.451Z","creation":"2025-04-05T11:45:38.451Z"},"accession":"S-EPMC10690942","cross_references":{"pubmed":["38045694"],"doi":["10.3389/fimmu.2023.1238457"]}}