ReviewThe Journal of clinical investigation2015
Genetic basis of autoimmunity.
Review in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 2 of them syntheses 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
66 citing papers in PubMed, 2 syntheses or guidelines pooled it, 118 citations in OpenAlex.
- TIM-3 rs1036199 polymorphism increases susceptibility to autoimmune diseases: evidence based on 4200 subjects.Bioscience reports · 2018Pooled it
- The Importance of Sex Stratification in Autoimmune Disease Biomarker Research: A Systematic Review.Frontiers in immunology · 2018Pooled it
- Cellular Stress and Immune Activation in Celiac Disease: Is the Chaperone System a Key Player?Biology · 2026Review
- Upadacitinib in rheumatoid arthritis: progress and challenges.Frontiers in pharmacology · 2026Review
- Mimicry in the Bite: Shared Sequences BetweenProteomes · 2025Article
- Review
- Acquired drivers of C3 glomerulopathy.Clinical kidney journal · 2025Review
- Occupational dust and chemical exposures and the development of autoimmune rheumatic diseases.Nature reviews. Rheumatology · 2025Review
- IKZF1 and UBR4 gene variants drive autoimmunity and Th2 polarization in IgG4-related disease.The Journal of clinical investigation · 2024Article
- Exposure to Environmental Toxins & Autoimmune Conditions.Integrative medicine (Encinitas, Calif.) · 2024Review
- Article
- Knowledge mapping of COVID-19 and autoimmune diseases: a visual and bibliometric analysis.Clinical and experimental medicine · 2023Article
- Autoimmune diseases and gut microbiota: a bibliometric and visual analysis from 2004 to 2022.Clinical and experimental medicine · 2023Article
- A novel hybrid model to predict concomitant diseases for Hashimoto's thyroiditis.BMC bioinformatics · 2023Article
- Clinical usefulness of anti-nuclear antibody in childhood: real-world experience at a tertiary care center : Usefulness of ANA in pediatric autoimmune diseases.European journal of pediatrics · 2023Article
- Genes and Microbiota Interaction in Monogenic Autoimmune Disorders.Biomedicines · 2023Review
- Benzo[a]pyrene Exposure Reduces Cell-Type Diversity and Stimulates Sex-Biased Damage Pathways in End Organs of Lupus-Prone Mice.International journal of molecular sciences · 2023Article
- Serum antinuclear autoantibodies are associated with measures of oxidative stress and lifestyle factors: analysis of LIPIDOGRAM2015 and LIPIDOGEN2015 studies.Archives of medical science : AMS · 2023Article
- The emerging role of noncoding RNAs in systemic lupus erythematosus: new insights into the master regulators of disease pathogenesis.Therapeutic advances in chronic disease · 2023Review
- The Anti-Inflammatory and Immunomodulatory Activities of Natural Products to Control Autoimmune Inflammation.International journal of molecular sciences · 2022Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Autoimmune diseases affect up to approximately 10% of the population. While rare Mendelian autoimmunity syndromes can result from monogenic mutations disrupting essential mechanisms of central and peripheral tolerance, more common human autoimmune diseases are complex disorders that arise from the interaction between polygenic risk factors and environmental factors. Although the risk attributable to most individual nucleotide variants is modest, genome-wide association studies (GWAS) have the potential to provide an unbiased view of biological pathways that drive human autoimmune diseases. Interpretation of GWAS requires integration of multiple genomic datasets including dense genotyping, cis-regulatory maps of primary immune cells, and genotyped studies of gene expression in relevant cell types and cellular conditions. Improved understanding of the genetic basis of autoimmunity may lead to a more sophisticated understanding of underlying cellular phenotypes and, eventually, novel diagnostics and targeted therapies.
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.