ReviewInternational immunology2016
Genetics of autoimmune diseases: perspectives from genome-wide association studies.
Review in International immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 4 of them syntheses that pooled it.
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.
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
40 citing papers in PubMed, 4 syntheses or guidelines pooled it.
- Therapeutic potential of natural coumarins in autoimmune diseases with underlying mechanisms.Frontiers in immunology · 2024Pooled it
- Association of NLRP3 rs35829419 and rs10754558 Polymorphisms With Risks of Autoimmune Diseases: A Systematic Review and Meta-Analysis.Frontiers in genetics · 2021Pooled it
- Meta-analyses of IL1A polymorphisms and the risk of several autoimmune diseases published in databases.PloS one · 2018Pooled it
- Association of XRCC1 Arg399Gln and Arg194Trp polymorphisms with susceptibility to multiple autoimmune diseases: a meta-analysis.Rheumatology international · 2017Pooled it
- Autoimmune disease: genetic susceptibility, environmental triggers, and immune dysregulation. Where can we develop therapies?Frontiers in immunology · 2025Review
- Protein-centric omics integration analysis identifies candidate plasma proteins for multiple autoimmune diseases.Human genetics · 2024Article
- Variants in the Late Cornified Envelope Gene Locus Are Associated With Elevated T-helper 17 Responses in Patients With Postinfectious Lyme Arthritis.The Journal of infectious diseases · 2024Article
- Article
- Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: the biology of a neglected disease.Frontiers in immunology · 2024Review
- Human Leukocyte Antigen B*27-Negative Spondyloarthritis: Clinical, Serological, and Radiological Features of a Single-Center Cohort.Diagnostics (Basel, Switzerland) · 2023Article
- Article
- Innate and adaptive immune abnormalities underlying autoimmune diseases: the genetic connections.Science China. Life sciences · 2023Review
- The Interplay of Transcription and Genome Topology Programs T Cell Development and Differentiation.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Antiviral Innate Immune Responses in Autoimmunity: Receptors, Pathways, and Therapeutic Targeting.Biomedicines · 2022Review
- Could the kynurenine pathway be the key missing piece of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) complex puzzle?Cellular and molecular life sciences : CMLS · 2022Review
- Association of a miRNA-binding site polymorphism in IL-16 gene with disease risk and clinical characteristics of rheumatoid arthritis and systemic lupus erythematosus.Clinical rheumatology · 2022Article
- HOTAIR and THRIL Long Non Coding RNAs and Their Target Genes in Rheumatoid Arthritis patients.Reports of biochemistry & molecular biology · 2022Article
- REVA as A Well-curated Database for Human Expression-modulating Variants.Genomics, proteomics & bioinformatics · 2021Article
- The multifaceted functional role of DNA methylation in immune-mediated rheumatic diseases.Clinical rheumatology · 2021Review
- Association study of genetic variants at TTC32-WDR35 gene cluster with coronary artery disease in Chinese Han population.Journal of clinical laboratory analysis · 2021Article
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genome-wide association studies (GWASs) for autoimmune diseases (ADs) have identified many risk loci and have provided insights into the etiology of each disease. Some of these loci, such asPTPN22,IL23RandSTAT4, are shared among different ADs, and the combination of risk loci may determine an individual's susceptibility for a disease. The majority of GWAS loci are expression quantitative trait loci (eQTLs), where disease-causing variants regulate expression of neighboring (or sometimes distant) genes. Because the eQTL effects are often cell type-specific, the incorporation of epigenetic data from disease-related cell types and tissues is expected to refine the identification of causal variants. The cumulative eQTL effects in multiple genes may influence the activity or fate of immune cells, which in turn may affect the function of the immune system in individuals. In this paper, I review the etiology of ADs by focusing on important immune cells (Th1 cells, Th17 cells and regulatory T cells), important pathways (antigen-receptor signaling and type I interferon signaling) and relevant genes identified in GWASs.
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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.