{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T05:39:32Z","timestamp":1791005972272,"version":"4.1.0"},"reference-count":48,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2024,1,11]],"date-time":"2024-01-11T00:00:00Z","timestamp":1704931200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>Observational studies found associations between ankylosing spondylitis (AS) and iridocyclitis (IC), but the causality remained unconfirmed.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We employed two-sample Mendelian randomization (MR) to investigate the bidirectional causal relationships between AS and IC. Single-nucleotide polymorphisms (SNPs) were chosen from the FinnGen database\u2019s genome-wide association studies (GWAS) following a rigorous evaluation of the studies\u2019 quality. Sensitivity analysis was performed to assess the potential influence of pleiotropy and heterogeneity on the MR findings.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Elevated genetic risk for AS showed positive causal effects on IC and its subtypes (IC, OR = 1.094, 95% CI = 1.035-1.157, <jats:italic>P<\/jats:italic> = 0.00156; Acute\/Subacute IC, OR = 1.327, 95% CI = 1.266-1.392, <jats:italic>P<\/jats:italic> = 8.73\u00d710<jats:sup>-32<\/jats:sup>; Chronic IC, OR = 1.454, 95% CI = 1.308-1.618, <jats:italic>P<\/jats:italic> = 5.19\u00d710<jats:sup>-12<\/jats:sup>). Significant causal association was specifically observed between Acute\/Subacute IC and AS (OR = 1.944, 95% CI = 1.316-2.873, <jats:italic>P<\/jats:italic> = 8.38\u00d710<jats:sup>-4<\/jats:sup>). Sensitivity analysis suggested that horizontal pleiotropy was unlikely to influence the causality, and the leave-one-out analysis confirmed that a single SNP did not drive the observed associations.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Our findings provide new proof of a positive causal relationship between AS and IC in the European population. Notably, it is Acute\/Subacute IC, rather than IC as a whole or Chronic IC, that is associated with an elevated risk of AS. These results emphasize the significance of considering AS characteristics in the diagnosis of Acute\/Subacute IC.<\/jats:p><\/jats:sec>","DOI":"10.3389\/fimmu.2023.1295118","type":"journal-article","created":{"date-parts":[[2024,1,11]],"date-time":"2024-01-11T04:15:45Z","timestamp":1704946545000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":3,"title":["Ankylosing spondylitis: acute\/subacute vs. chronic iridocyclitis - a bidirectional two-sample Mendelian randomization study"],"prefix":"10.3389","volume":"14","author":[{"given":"Hui","family":"Li","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yingying","family":"Xu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qin","family":"Guo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tiantian","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shufen","family":"Zhou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Meimei","family":"Wu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuanxiong","family":"Cheng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chengshan","family":"Guo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2024,1,11]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"73","DOI":"10.1016\/S0140-6736(16)31591-4","article-title":"Axial spondyloarthritis","volume":"390","author":"Sieper","year":"2017","journal-title":"Lancet"},{"key":"B2","doi-asserted-by":"publisher","first-page":"m4447","DOI":"10.1136\/bmj.m4447","article-title":"Axial spondyloarthritis: new advances in diagnosis and management","volume":"372","author":"Ritchlin","year":"2021","journal-title":"BMJ"},{"key":"B3","article-title":"Incidence and prevalence of axial spondyloarthritis: methodologic challenges and gaps in the literature","volume":"36","author":"Bohn","year":"2018","journal-title":"Clin Exp Rheumatol"},{"key":"B4","doi-asserted-by":"publisher","first-page":"81","DOI":"10.1038\/nrrheum.2015.133","article-title":"Genetics of ankylosing spondylitis\u2013insights into pathogenesis","volume":"12","author":"Brown","year":"2016","journal-title":"Nat Rev Rheumatol"},{"key":"B5","doi-asserted-by":"publisher","first-page":"296","DOI":"10.1038\/nrrheum.2012.41","article-title":"Genetics of spondyloarthritis\u2013beyond the mhc","volume":"8","author":"Reveille","year":"2012","journal-title":"Nat Rev Rheumatol"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/nrrheum.2017.56","article-title":"Pathogenesis of ankylosing spondylitis - 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