ArticleNature communications2023
Cross-disorder genetic analysis of immune diseases reveals distinct gene associations that converge on common pathways.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed.
- Tissue-specific clustering of genetic correlations across autoimmune diseases in a nationwide sibling study.The Journal of clinical investigation · 2026Article
- Revealing the Shared Genetic Architecture of Metabolic Dysfunction-Associated Steatotic Liver Disease-Related Traits Through Genomic Structural Equation Modeling.Genetic epidemiology · 2026Article
- Endothelial Collapse as a Convergent Immunovascular Phenotype in Sepsis and Severe Arboviral Disease: The SIMVAC Model.Pathogens (Basel, Switzerland) · 2026Review
- Post-genome-wide association study variant-to-function challenges in asthma research.The Journal of allergy and clinical immunology · 2026Review
- Dissecting pleiotropy between major depressive disorder and physical disease comorbidities.Nature genetics · 2026Article
- Multi-omics-driven precision medicine.iMeta · 2026Review
- Murine and Humanized Mouse Models in Autoimmune Disease Research and Therapeutics Development.Biology · 2026Review
- Transcription-based identification of uncharacterized genes in the human immune response.European journal of human genetics : EJHG · 2026Article
- Cross-trait mapping of shared susceptibility across inflammatory bowel disease and spondyloarthropathies.Journal of translational medicine · 2026Article
- Glycoproteomic and genetic analysis of N-glycosylation of complement component C3 reveals immune pathway regulation.Genome biology · 2026Article
- eQTL analysis: A bridge from genome to mechanism.Genes & diseases · 2026Review
- Multivariate genetic analysis reveals three distinct pathological dimensions in musculoskeletal disorders.Nature communications · 2026Article
- Dissecting pleiotropy to gain mechanistic insights into human disease.Nature reviews. Genetics · 2026Review
- Genomic Structural Equation Modeling Reveals Cardiovascular-Kidney-Metabolic Syndrome Genetic Architecture.Journal of diabetes · 2026Article
- Identifying genetic and cellular connections and distinctions among 15 autoimmune diseases using an in-silico approach.Communications medicine · 2026Article
- PGVDA: a pathway-aggregated genetic dosage framework for interpretable disease classification using machine learning.Briefings in bioinformatics · 2026Article
- Identifying a Common Autoimmune Gene Core as a Tool for Verifying Biological Significance and Applicability of Polygenic Risk Scores.International journal of molecular sciences · 2026Article
- Integrating genomic structural equation modeling and experimental validation to unravel the genetic basis of male genital lichen sclerosus.Frontiers in immunology · 2026Article
- Timing matters in diagnosis of cancer with immune-mediated inflammatory disease.Nature reviews. Rheumatology · 2025Article
- Preclinical Diagnosis of Type 1 Diabetes: Reality or Utopia.Biomedicines · 2025Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genome-wide association studies (GWAS) have mapped thousands of susceptibility loci associated with immune-mediated diseases. To assess the extent of the genetic sharing across nine immune-mediated diseases we apply genomic structural equation modelling to GWAS data from European populations. We identify three disease groups: gastrointestinal tract diseases, rheumatic and systemic diseases, and allergic diseases. Although loci associated with the disease groups are highly specific, they converge on perturbing the same pathways. Finally, we test for colocalization between loci and single-cell eQTLs derived from peripheral blood mononuclear cells. We identify the causal route by which 46 loci predispose to three disease groups and find evidence for eight genes being candidates for drug repurposing. Taken together, here we show that different constellations of diseases have distinct patterns of genetic associations, but that associated loci converge on perturbing different nodes in T cell activation and signalling pathways.
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