ArticleJournal of autoimmunity2016
Refined mapping of autoimmune disease associated genetic variants with gene expression suggests an important role for non-coding RNAs.
Article in Journal of autoimmunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.
- Integration ofFrontiers in immunology · 2023Pooled it
- Crosstalk between inflammation and autophagy in CeD organoids.Scientific reports · 2026Article
- eQTL in diseased colon tissue identifies potential target genes associated with IBD.Nature communications · 2026Article
- Transcriptomics and eQTLs reveal inflammatory heterogeneity in the duodenal lining in coeliac disease.Genes and immunity · 2025Article
- An inflammation-associated lncRNA induces neuronal damage via mitochondrial dysfunction.Molecular therapy. Nucleic acids · 2025Article
- Review
- Fine-mapping and molecular characterisation of primary sclerosing cholangitis genetic risk loci.Nature communications · 2024Article
- Article
- Investigating shared genetic architecture between inflammatory bowel diseases and primary biliary cholangitis.JHEP reports : innovation in hepatology · 2024Article
- mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- From an understanding of etiopathogenesis to novel therapies-what is new in the treatment of celiac disease?Frontiers in pharmacology · 2024Review
- Autoimmunity-related LINC01934 and AP002954.4 lncRNA polymorphisms may be effective in pediatric celiac disease: a case-control study.Revista da Associacao Medica Brasileira (1992) · 2024Article
- Orphan G protein-coupled receptors: the ongoing search for a home.Frontiers in pharmacology · 2024Review
- Identifying platelet-derived factors as amplifiers of B. burgdorferi-induced cytokine production.Clinical and experimental immunology · 2022Article
- Impact of Multiple Sclerosis Risk Polymorphism rs7665090 on MANBA Activity, Lysosomal Endocytosis, and Lymphocyte Activation.International journal of molecular sciences · 2022Article
- Unraveling the Influence ofInternational journal of molecular sciences · 2022Article
- Celiac disease: From genetics to epigenetics.World journal of gastroenterology · 2022Review
- Gluten-induced RNA methylation changes regulate intestinal inflammation via allele-specificGut · 2022Article
- Single-Cell RNA Sequencing of Peripheral Blood Mononuclear Cells From Pediatric Coeliac Disease Patients Suggests Potential Pre-Seroconversion Markers.Frontiers in immunology · 2022Article
- Small RNA Expression Profiling Reveals hsa-miR-181d-5p Downregulation Associated With TNF-α Overexpression in Sjögren's Syndrome Patients.Frontiers in immunology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
25 authors at 4 institutions in 3 countries.
Funding
Abstract
Genome-wide association and fine-mapping studies in 14 autoimmune diseases (AID) have implicated more than 250 loci in one or more of these diseases. As more than 90% of AID-associated SNPs are intergenic or intronic, pinpointing the causal genes is challenging. We performed a systematic analysis to link 460 SNPs that are associated with 14 AID to causal genes using transcriptomic data from 629 blood samples. We were able to link 71 (39%) of the AID-SNPs to two or more nearby genes, providing evidence that for part of the AID loci multiple causal genes exist. While 54 of the AID loci are shared by one or more AID, 17% of them do not share candidate causal genes. In addition to finding novel genes such as ULK3, we also implicate novel disease mechanisms and pathways like autophagy in celiac disease pathogenesis. Furthermore, 42 of the AID SNPs specifically affected the expression of 53 non-coding RNA genes. To further understand how the non-coding genome contributes to AID, the SNPs were linked to functional regulatory elements, which suggest a model where AID genes are regulated by network of chromatin looping/non-coding RNAs interactions. The looping model also explains how a causal candidate gene is not necessarily the gene closest to the AID SNP, which was the case in nearly 50% of cases.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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 OpenQuestion graph.