{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,13]],"date-time":"2026-09-13T03:47:33Z","timestamp":1789271253839,"version":"build-2803163510"},"reference-count":74,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2025,10,31]],"date-time":"2025-10-31T00:00:00Z","timestamp":1761868800000},"content-version":"vor","delay-in-days":303,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,1,1]],"date-time":"2025-01-01T00:00:00Z","timestamp":1735689600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Mediators of Inflammation"],"published-print":{"date-parts":[[2025,1]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Clinical evidence indicates that inflammatory bowel disease (IBD) and ankylosing spondylitis (AS) often co\u2010occur, but their genetic mechanisms remain unclear. Our objective is to explore the genetic relationship between IBD and AS.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Using large\u2010scale summary statistics from genome\u2010wide association study (GWAS), we investigated the shared genetic architecture between IBD, including ulcerative colitis (UC) and Crohn\u2019s disease (CD), and AS. Starting with genetic correlation, we then examined shared genetic structures and genes, followed by causal inference, and explored potential functional genes and biological pathways in tissue and cell types.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We observed a positive genetic correlation between IBD and AS (IBD\u2013AS:\n                      <jats:italic>r<\/jats:italic>\n                      <jats:sub>\n                        <jats:italic>g<\/jats:italic>\n                      <\/jats:sub>\n                      \u2009=\u20090.252,\n                      <jats:italic>p<\/jats:italic>\n                      = 3.78e \u2212 06; CD\u2013AS:\n                      <jats:italic>r<\/jats:italic>\n                      <jats:sub>\n                        <jats:italic>g<\/jats:italic>\n                      <\/jats:sub>\n                      \u2009=\u20090.268,\n                      <jats:italic>p<\/jats:italic>\n                      = 5.19e \u2212 06; UC\u2013AS:\n                      <jats:italic>r<\/jats:italic>\n                      <jats:sub>\n                        <jats:italic>g<\/jats:italic>\n                      <\/jats:sub>\n                      \u2009=\u20090.171,\n                      <jats:italic>p<\/jats:italic>\n                      = 6.64e \u2212 03). Multitrait analysis of GWAS (MTAG) and cross\u2010phenotype association analysis (CPASSOC) identified 24 pleiotropic single\u2010nucleotide polymorphisms (SNPs) across three trait pairs. Gene association analysis from three methods collectively identified eight shared functional genes for IBD and AS. Shared tissue\u2010specific genetic enrichment was found in lung, spleen, small intestine, and whole blood tissues. Additionally, common enrichment was observed in specific cell types, such as T and B cells. Bidirectional Mendelian randomization (MR) analysis revealed no causal relationship between the two conditions.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>This study confirms the genetic correlation between IBD and AS, identifies their shared genetic architecture and biological pathways, providing strong evidence for the genetic comorbidity of IBD and AS. These findings offer directions for future research.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1155\/mi\/4012195","type":"journal-article","created":{"date-parts":[[2025,10,31]],"date-time":"2025-10-31T07:51:31Z","timestamp":1761897091000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["A Multitrait Analysis of Genome\u2010Wide Association Study Reveals the Shared Genetic Architecture Between Inflammatory Bowel Disease and Ankylosing Spondylitis"],"prefix":"10.1155","volume":"2025","author":[{"given":"Hongyan","family":"Li","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dadong","family":"Tang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yanling","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qijie","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0000-9706-2109","authenticated-orcid":false,"given":"Hongchang","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2025,10,31]]},"reference":[{"key":"e_1_2_11_1_2","doi-asserted-by":"publisher","DOI":"10.1038\/nature10209"},{"key":"e_1_2_11_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ccm.2019.05.006"},{"key":"e_1_2_11_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrgastro.2015.208"},{"key":"e_1_2_11_4_2","doi-asserted-by":"publisher","DOI":"10.1080\/17474124.2019.1574569"},{"key":"e_1_2_11_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.berh.2006.03.010"},{"key":"e_1_2_11_6_2","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2024.1326354"},{"key":"e_1_2_11_7_2","first-page":"226","article-title":"Exploring 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