ReviewNature reviews. Endocrinology2013
GWAS in autoimmune thyroid disease: redefining our understanding of pathogenesis.
Review in Nature reviews. Endocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 4 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
63 citing papers in PubMed, 4 syntheses or guidelines pooled it, 123 citations in OpenAlex.
- Epigenome-wide Association Study Shows Differential DNA Methylation of MDC1, KLF9, and CUTA in Autoimmune Thyroid Disease.The Journal of clinical endocrinology and metabolism · 2024Pooled it
- Prevalence of autoimmune thyroid disease in patients with psoriasis: a meta-analysis.BMJ open · 2022Pooled it
- Genetic associations of the thyroid stimulating hormone receptor gene with Graves diseases and Graves ophthalmopathy: A meta-analysis.Scientific reports · 2016Pooled it
- Identification of novel genetic Loci associated with thyroid peroxidase antibodies and clinical thyroid disease.PLoS genetics · 2014Pooled it
- The Footprints of Poly-Autoimmunity: Evidence for Common Biological Factors Involved in Multiple Sclerosis and Hashimoto's Thyroiditis.Frontiers in immunology · 2018Trial
- Article
- Single-Cell RNA Sequencing of Thyroid Tissues Reveals Pathogenesis of Graves' Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Haplotype analysis reveals pleiotropic disease associations in the HLA region.American journal of human genetics · 2025Article
- Clonal hematopoiesis of indeterminate potential and risk of autoimmune thyroid disease.BMC medicine · 2025Article
- Graves' Disease: Is It Time for Targeted Therapy? A Narrative Review.Medicina (Kaunas, Lithuania) · 2025Review
- Association Between FOXP3 rs2232368 Variant and Hashimoto's Thyroiditis Risk: A Case-Control Study.Cureus · 2025Article
- Role of the suppressor of cytokine signaling-3 in the pathogenesis of Graves' orbitopathy.Frontiers in endocrinology · 2025Article
- Occupational Physical Activity and Regular Exercise Are Inversely Correlated with Thyroid Function in Patients with Hashimoto's Thyroiditis.Diseases (Basel, Switzerland) · 2024Article
- Graves disease: latest understanding of pathogenesis and treatment options.Nature reviews. Endocrinology · 2024Review
- Associations between immune cell traits and autoimmune thyroid diseases: a bidirectional two-sample mendelian randomization study.Immunogenetics · 2024Article
- Autoimmune Hemolytic Anemia with Autoimmune Hypothyroidism: A Case Report.JNMA; journal of the Nepal Medical Association · 2023Article
- Identification of multiple novel susceptibility genes associated with autoimmune thyroid disease.Frontiers in immunology · 2023Article
- Genome-wide DNA methylation pattern in whole blood of patients with Hashimoto thyroiditis.Frontiers in endocrinology · 2023Article
- Iron: Not Just a Passive Bystander in AITD.Nutrients · 2022Review
- Peripheral immunophenotyping of AITD subjects reveals alterations in immune cells in pediatric vs adult-onset AITD.iScience · 2022Article
3 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
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ability of the immune system to protect the body from attack by foreign antigens is essential for human survival. The immune system can, however, start to attack the body's own organs. An autoimmune response against components of the thyroid gland affects 2-5% of the general population. Considerable familial clustering is also observed in autoimmune thyroid disease (AITD). Teasing out the genetic contribution to AITD over the past 40 years has helped unravel how immune disruption leads to disease onset. Breakthroughs in genome-wide association studies (GWAS) in the past decade have facilitated screening of a greater proportion of the genome, leading to the identification of a before unimaginable number of AITD susceptibility loci. This Review will focus on the new susceptibility loci identified by GWAS, what insights these loci provide about the pathogenesis of AITD and how genetic susceptibility loci shared between different autoimmune diseases could help explain disease co-clustering within individuals and families. This Review also discusses where future efforts should be focused to translate this step forward in our understanding of the genetic contribution to AITD into a better understanding of disease presentation and progression, and improved therapeutic options.
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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.