SynthesisFrontiers in immunology2026
Multi-layered functional genomics prioritizes candidate effectors and regulatory mechanisms of ankylosing spondylitis.
Synthesis in Frontiers in immunology, 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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Abstract
Background: Ankylosing spondylitis (AS) is a chronic inflammatory arthropathy with heritability estimated at approximately 90%, yet the effector genes and regulatory mechanisms beyond the well-established Methods: We performed a GWAS meta-analysis of 7,551 AS cases and 1,258,581 controls from the Million Veteran Program, FinnGen, and UK Biobank whole-genome sequencing cohorts. The post-GWAS analysis combined causal transcriptome-wide association study (cTWAS) across four immune-relevant tissues, colocalization, four-method fine-mapping, Geneformer V2 in-silico perturbation, AlphaGenome variant-effect prediction, cross-trait LD-score regression (LDSC), pathway enrichment, structured druggability assessment, and siRNA knockdown in Jurkat T cells. We added LDSC calibration, per-cohort Q-Q plots, heterogeneity summaries, and leave-one-cohort-out sensitivity analyzes for revised quality control. Results: The meta-analysis identified 30 genome-wide significant loci harboring 26,178 significant variants. After LDSC-compatible quality control, the meta-analysis showed lambda_GC = 1.09, LDSC intercept = 1.045 (SE = 0.009), and attenuation ratio = 0.365 (SE = 0.075); per-cohort lambda_GC values were 1.027, 1.080, and 1.018 for MVP, FinnGen, and UKB-WGS, respectively. cTWAS prioritized 64 causal-candidate genes (posterior inclusion probability [PIP] > 0.5), with gene expression explaining 19.5% of AS heritability. Seven genes showed convergent cTWAS and colocalization evidence ( Conclusions: This convergent evidence framework prioritizes AS candidate genes and regulatory variants while separating statistical prioritization from experimental support. The revised analyzes strengthen calibration, heterogeneity reporting, cross-disease context, and translational interpretation, nominating immune and regulatory hypotheses for follow-up rather than definitive therapeutic targets.
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