ReviewImmunologic research2012
Delineating the autoimmune mechanisms in Graves' disease.
Review in Immunologic research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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
61 citing papers in PubMed, 130 citations in OpenAlex.
- Trial
- Machine learning in lymphocyte and immune biomarker analysis for childhood thyroid diseases in China.BMC pediatrics · 2025Article
- Role of the suppressor of cytokine signaling-3 in the pathogenesis of Graves' orbitopathy.Frontiers in endocrinology · 2025Article
- Expression levels of T cell-related immune factors and their correlation with thyroid function in Graves' disease with varied serum iodine status: insights into immunopathogenesis.Frontiers in endocrinology · 2025Article
- Article
- HLA Class II Allele Groups Involved in Autoimmune Thyroid Diseases: Hashimoto's Thyroiditis and Basedow-Graves Disease.Life (Basel, Switzerland) · 2024Article
- Article
- Graves disease is associated with increased risk of clinical Alzheimer's disease: evidence from the Medicare system.Clinical diabetes and endocrinology · 2024Article
- Article
- Association between small intestine bacterial overgrowth and psychiatric disorders.Frontiers in endocrinology · 2024Review
- Innate Immunity in Autoimmune Thyroid Disease during Pregnancy.International journal of molecular sciences · 2023Review
- Graves Disease is Associated with Increased Risk of Clinical Alzheimer's Disease: Evidence from the Medicare System.Research square · 2023Article
- Allosteric Regulation of G-Protein-Coupled Receptors: From Diversity of Molecular Mechanisms to Multiple Allosteric Sites and Their Ligands.International journal of molecular sciences · 2023Review
- Structure of full-length TSH receptor in complex with antibody K1-70™.Journal of molecular endocrinology · 2023Article
- New insight into the causal relationship between Graves' disease liability and drug eruption: a Mendelian randomization study.Frontiers in immunology · 2023Article
- Long-term management of Graves disease: a narrative review.Journal of Yeungnam medical science · 2023Article
- Article
- A glance at post-translational modifications of human thyroglobulin: potential impact on function and pathogenesis.European thyroid journal · 2022Review
- SARS-CoV-2 triggering autoimmune diseases.Cytokine · 2022Review
- Review
1 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 2 institutions in 1 country.
Funding
Abstract
The immunologic processes involved in autoimmune thyroid disease (AITD), particularly Graves' disease (GD), are similar to other autoimmune diseases with the emphasis on the antibodies as the most unique aspect. These characteristics include a lymphocytic infiltrate at the target organs, the presence of antigen-reactive T and B cells and antibodies, and the establishment of animal models of GD by antibody transfer or immunization with antigen. Similar to other autoimmune diseases, risk factors for GD include the presence of multiple susceptibility genes, including certain HLA alleles, and the TSHR gene itself. In addition, a variety of known risk factors and precipitators have been characterized including the influence of sex and sex hormones, pregnancy, stress, infection, iodine and other potential environmental factors. The pathogenesis of GD is likely the result of a breakdown in the tolerance mechanisms, both at central and peripheral levels. Different subsets of T and B cells together with their regulatory populations play important roles in the propagation and maintenance of the disease process. Understanding different mechanistic in the complex system biology interplay will help to identify unique factors contributing to the AITD pathogenesis.
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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.