SynthesisFrontiers in immunology2025
Genetic architecture of primary biliary cholangitis: strong evidence for HLA and non-HLA risk loci.
Synthesis in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Novel Mechanistic Insights into Primary Biliary Cholangitis: From Pathogenesis to Mesenchymal Stem Cell-Mediated Repair.Biomedicines · 2026Review
- Human leukocyte antigen variants and clinical features of primary biliary cholangitis: Cumulative contributions.World journal of clinical cases · 2026Article
- Breaking the metabolo-immune cycle in primary biliary cholangitis for therapeutic benefit.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Despite extensive genetic studies investigating primary biliary cholangitis (PBC), the mechanistic basis of risk-associated variants remains poorly understood. To address this gap, we performed a systematic evaluation of cumulative evidence linking genetic variants to PBC susceptibility. Methods: A comprehensive search was conducted to identify published studies on the association between genetic variants and PBC risk. Specifically, separate analyses were conducted for genome-wide association studies (GWASs) and candidate-gene association studies to address potential heterogeneity arising from differences in study design. Meta-analyses were performed to calculate pooled odds ratio (OR) and 95% confidence interval (CI) for the candidate-gene association studies. Significant associations were further graded using Venice criteria and false-positive report probability (FPRP) tests. Functional annotation, pathway enrichment, and phenome-wide analyses were performed to elucidate biological relevance. Results: Overall, we included 105 articles involving 71,031 cases and 140,499 controls. Meta-analyses were conducted for 70 variants across 33 genes. Among these, 44 variants were identified as significantly associated with PBC risk, comprising 30 HLA variants and 14 non-HLA variants. Separately, published GWAS have reported 115 significant variants. Nine variants (DQA1*0401, DQB1*0301, DQB1*0402, DQB1*0602, DRB1*08, DRB1*0803, DRB1*11, DRB1*1101, and rs7574865) were identified by both approaches. Additionally, meta-analyses of candidate-gene association studies provided strong evidence supporting the association of eight further variants (A*3303, B*4403, DPB1*0201, DQB1*0401, rs231725, rs231775, rs1544410, and rs9303277) with PBC at the genome-wide significance level ( Conclusion: This study provides the most comprehensive synopsis to date of PBC's genetic architecture, highlighting robust HLA and non-HLA risk loci. Systematic review registration: https:///www.crd.york.ac.uk/PROSPERO/view/CRD42021282146, identifier CRD42021282146.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.