<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>14</volume><submitter>Cai Y</submitter><pubmed_abstract>&lt;h4>Introduction&lt;/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.&lt;h4>Methods&lt;/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.&lt;h4>Results&lt;/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 &lt; 0.01; IL-17E: OR: 1.17, 95% CI, 1.05-1.30, P &lt; 0.01; IL-17RB: OR: 1.30, 95% CI, 1.20-1.40, P &lt; 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 &lt; 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.&lt;h4>Discussion&lt;/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.</pubmed_abstract><journal>Frontiers in immunology</journal><pagination>1238457</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10690942</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Interleukin-17 and inflammatory bowel disease: a 2-sample Mendelian randomization study.</pubmed_title><pmcid>PMC10690942</pmcid><pubmed_authors>Xu L</pubmed_authors><pubmed_authors>Cai J</pubmed_authors><pubmed_authors>Cai Y</pubmed_authors><pubmed_authors>Jia X</pubmed_authors><pubmed_authors>Chen H</pubmed_authors><pubmed_authors>Xie S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Interleukin-17 and inflammatory bowel disease: a 2-sample Mendelian randomization study.</name><description>&lt;h4>Introduction&lt;/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.&lt;h4>Methods&lt;/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.&lt;h4>Results&lt;/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 &lt; 0.01; IL-17E: OR: 1.17, 95% CI, 1.05-1.30, P &lt; 0.01; IL-17RB: OR: 1.30, 95% CI, 1.20-1.40, P &lt; 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 &lt; 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.&lt;h4>Discussion&lt;/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.</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023</publication><modification>2025-04-05T11:45:38.451Z</modification><creation>2025-04-05T11:45:38.451Z</creation></dates><accession>S-EPMC10690942</accession><cross_references><pubmed>38045694</pubmed><doi>10.3389/fimmu.2023.1238457</doi></cross_references></HashMap>