ArticleJournal of translational medicine2026
Cross-trait mapping of shared susceptibility across inflammatory bowel disease and spondyloarthropathies.
Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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6 authors.
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Abstract
backgroundInflammatory bowel diseases (IBDs) and spondyloarthropathies (SpAs) frequently co-occur, yet the subtype-specific genetic architecture and effector tissues that implement this gut-joint coupling remain poorly defined.
methodsWe integrated European-ancestry GWAS summary statistics for IBD, Crohn's disease, ulcerative colitis, ankylosing spondylitis, psoriatic arthritis, reactive arthritis and enteropathic arthritis, covering 22.21 million variants across 1,263,767 individuals. We quantified genome-wide and local sharing (S-LDSC/LDSC, ρ-HESS), identified pleiotropic loci (MTAG, CPASSOC) in trait pairs with significant genome-wide genetic correlation, and prioritized shared loci by integrating local-correlation evidence with GWAS-PW and GCTA-COJO, mapped signals to tissues/cell types (LDSC-SEG, gsMap), prioritized effector genes (UTMOST, FUSION, SMR, immune-cell scPrediXcan), and assessed directionality using bidirectional Mendelian randomization.
resultsIBD showed 16.4% liability-scale SNP heritability (CD 21.5%; UC 15.2%), whereas SpA subtype heritability ranged from 2.4% (ReA) to 62.9% (AS). Genetic correlations were positive but heterogeneous, with the strongest sharing observed for EnA-related pairs. Local genetic analyses indicated structured but uneven regional sharing across subtype pairs, with the most robust local support concentrated in PsA- and EnA-related comparisons. Tissue and cell-type analyses converged mainly on immune- and barrier-related contexts, including blood, synovial fluid, spleen, lung, and lymphoid tissues, as well as T-lineage and myeloid immune compartments. Complementary gsMap projection suggested a developmentally informed gut-immune spatial scaffold rather than a uniform anatomical pattern. Pair-specific transcriptomic integration further prioritized recurrent candidate effectors across the IBD-SpA axis, while bidirectional Mendelian randomization supported a predominantly forward component from intestinal inflammatory liability to selected SpA phenotypes.
conclusionThese results provide a multi-layer genetic and biological framework for gut-joint comorbidity, implicating shared immune and barrier niches and supporting a gut-first component in the IBD-SpA axis.
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