ReviewThyroid : official journal of the American Thyroid Association2008
Cytokines, Graves' disease, and thyroid-associated ophthalmopathy.
Review in Thyroid : official journal of the American Thyroid Association, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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
53 citing papers in PubMed, 140 citations in OpenAlex.
- c-FLIP as a master regulator of immune homeostasis and disease mechanisms.Cell death & disease · 2026Review
- Article
- Peripheral CD3Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2024Article
- A comprehensive epigenetic network can influence the occurrence of thyroid-associated ophthalmopathy by affecting immune and inflammatory response.Scientific reports · 2024Article
- Smoking enhances proliferation, inflammatory markers, and immunoglobulins in peripheral blood mononuclear cells from Graves' patients.Endocrine connections · 2024Article
- CD169iScience · 2024Article
- Evaluating the causal effects between Grave's disease and diabetes mellitus: a bidirectional Mendelian randomization study.Frontiers in endocrinology · 2024Article
- A combined transcriptomics and proteomics approach reveals S100A4 as a potential biomarker for Graves' orbitopathy.Frontiers in genetics · 2024Article
- Early life stress in women with autoimmune thyroid disorders.Scientific reports · 2023Article
- Evaluation of Epithelial-Mesenchymal Transition Markers in Autoimmune Thyroid Diseases.International journal of molecular sciences · 2023Article
- TSG6 Plays a Role in Improving Orbital Inflammatory Infiltration and Extracellular Matrix Accumulation in TAO Model Mice.Journal of inflammation research · 2023Article
- HbA1c: an independent risk factor for dysthyroid optic neuropathy.Frontiers in endocrinology · 2023Article
- Graves' disease as a driver of depression: a mechanistic insight.Frontiers in endocrinology · 2023Review
- Tears as a Source of Biomarkers in the Diagnosis of Graves' Orbitopathy.Biomolecules · 2022Review
- Optic nerve head optical coherence tomography angiography findings in patients with thyroid eye disease: a case-control study.Thyroid research · 2022Article
- The role of IL-6 and osteoprotegerin in bone metabolism in patients with Graves' disease.Turkish journal of medical sciences · 2022Article
- Role of the mononuclear cell infiltrate in Graves' orbitopathy (GO): results of a large cohort study.Journal of endocrinological investigation · 2022Observational
- Thyroid function in COVID-19 and the association with cytokine levels and mortality.Endocrine connections · 2021Article
- Differential expression and alternative splicing of transcripts in orbital adipose/connective tissue of thyroid-associated ophthalmopathy.Experimental biology and medicine (Maywood, N.J.) · 2021Article
- TGF-β Physiology as a Novel Therapeutic Target Regarding Autoimmune Thyroid Diseases: Where Do We Stand and What to Expect.Medicina (Kaunas, Lithuania) · 2021Review
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
Graves' disease, an autoimmune process associated with thyroid dysfunction, can also manifest as remodeling of orbital connective tissue. Affected tissues exhibit immune responses that appear to be orchestrated by resident cells and those recruited from the bone marrow through their expression and release of cytokines and surface display of cytokine receptors. Cytokines are small molecules produced by many types of cells, including those of the "professional" immune system. Aberrant cytokine expression appears to play an important role in the pathogenesis of many human diseases, including thyroid autoimmunity. The skewed pattern of cytokine expression in the thyroid, including the T helper cell bias, may condition the response to apoptotic signals and determine the characteristics of an autoimmune reaction. Furthermore, chemoattractant cytokines, including IL16, RANTES, and CXCL10, elaborated by resident cells in the thyroid and orbit may provoke mononuclear cell infiltration. Other cytokines may drive cell activation and tissue remodeling. Thus cytokines and the signaling pathways they activate represent attractive therapeutic targets. Interruption of these might alter the natural course of Graves' disease and its orbital 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.