ReviewMediators of inflammation2017
General and Specific Genetic Polymorphism of Cytokines-Related Gene in AITD.
Review in Mediators of inflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 3 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
18 citing papers in PubMed, 3 syntheses or guidelines pooled it, 35 citations in OpenAlex.
- Causal relationship between inflammatory cytokines and autoimmune thyroid disease: a bidirectional two-sample Mendelian randomization analysis.Frontiers in immunology · 2024Pooled it
- Immune Checkpoint Inhibitors-Related Thyroid Dysfunction: Epidemiology, Clinical Presentation, Possible Pathogenesis, and Management.Frontiers in endocrinology · 2021Pooled it
- Association between thyroglobulin polymorphisms and autoimmune thyroid disease: a systematic review and meta-analysis of case-control studies.Genes and immunity · 2019Pooled it
- Clonal hematopoiesis of indeterminate potential and risk of autoimmune thyroid disease.BMC medicine · 2025Article
- Autoimmune Thyroid Disease and Pregnancy: The Interaction Between Genetics, Epigenetics and Environmental Factors.Journal of clinical medicine · 2024Review
- Unraveling the molecular architecture of autoimmune thyroid diseases at spatial resolution.Nature communications · 2024Article
- The association of common autoimmune diseases with autoimmune thyroiditis: a two-sample Mendelian randomization study.Frontiers in endocrinology · 2024Article
- Review
- Evaluation of Epithelial-Mesenchymal Transition Markers in Autoimmune Thyroid Diseases.International journal of molecular sciences · 2023Article
- B cells from anti-thyroid antibody positive, infertile women show hyper-reactivity to BCR stimulation.Frontiers in immunology · 2022Article
- The Epidemiological Characteristics of Autoimmune Thyroiditis in the Tuzla Canton in the Period from 2015 to 2020.Materia socio-medica · 2021Article
- Predisposition to Graves' disease and Graves' ophthalmopathy by genetic variants of IL2RA.Journal of molecular medicine (Berlin, Germany) · 2021Article
- A data-driven approach for the discovery of biomarkers associated with thyroid eye disease.BMC ophthalmology · 2021Article
- Genetics, Epigenetics, Cellular Immunology, and Gut Microbiota: Emerging Links With Graves' Disease.Frontiers in cell and developmental biology · 2021Review
- Genetic Susceptibility to Joint Occurrence of Polycystic Ovary Syndrome and Hashimoto's Thyroiditis: How Far Is Our Understanding?Frontiers in immunology · 2021Review
- Sjögren's Syndrome and Autoimmune Thyroid Disease: Two Sides of the Same Coin.Clinical reviews in allergy & immunology · 2019Article
- Genome-wide association analysis suggests novel loci for Hashimoto's thyroiditis.Journal of endocrinological investigation · 2019Article
- Copy Number Variation of Immune-Related Genes and Their Association with Iodine in Adults with Autoimmune Thyroid Diseases.International journal of endocrinology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autoimmune thyroid disease (AITD) shows the highest incidence among organ-specific autoimmune diseases and is the most common thyroid disease in humans, including Graves' disease (GD) and Hashimoto's thyroiditis (HT). The susceptibility to autoimmune diseases is affected by increased autoantibody levels, susceptibility gene polymorphisms, environmental factors, and psychological factors, but the pathogenesis remains unclear. Various cytokines and related genes encoding them play important roles in the development and progression of AITD. CD152, an expression product of the CTLA-4 gene, downregulates T cell activation. The A/A genotype polymorphism in the CT60 locus may reduce the production of thyroid autoantibodies. The C1858T polymorphism of the PTNP22 gene reduces the expression of its encoded LYP, which increases the risk of GD and HT. GD is an organ-specific autoimmune disease involving increased secretion of thyroid hormone, whereas HT may be associated with the destruction of thyroid gland tissue and hypothyroidism. These two diseases exhibit similar pathogenesis but opposite trends in the clinical manifestations. In this review, we focus on the structure and function of these cytokines and related genes in AITD, as well as the association of polymorphisms with susceptibility to GD and HT, and attempt to describe their differences in pathogenesis and clinical manifestations.
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.