Evidence map›Paper›PMID 41243116›Full record

SynthesisAnnals of medicine2025

Role of interleukin 17 and T helper cells 17 cells as a new immune target and signalling in the pathogenesis and treatment of autoimmune thyroid diseases.

Huihong He, Yuancong Jiang, Jie Qiu, Fengqing Shen, Da Qian, Liwei Meng

Abstract readSystematic Review
In one paragraph

Synthesis in Annals of medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
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  5. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Huihong HeDepartment of Breast and Thyroid Surgery, Shaoxing People's Hospital, Shaoxing, China.
Yuancong JiangDepartment of Breast and Thyroid Surgery, Shaoxing People's Hospital, Shaoxing, China.
Jie QiuDepartment of Breast and Thyroid Surgery, Shaoxing People's Hospital, Shaoxing, China.
Fengqing ShenDepartment of Breast and Thyroid Surgery, Shaoxing People's Hospital, Shaoxing, China.
Da QianCentral Laboratory, Department of Scientific Research, Changshu Hospital Affiliated to Soochow University, Changshu, China.ORCID 0000-0002-6062-8161
Liwei MengDepartment of Breast and Thyroid Surgery, Shaoxing People's Hospital, Shaoxing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThis study aims to systematically review the molecular and cellular mechanisms by which the interleukin 17 (IL-17)/T helper cells (Th17) signalling axis contributes to Graves' disease (GD) and Hashimoto's thyroiditis (HT), with particular focus on IL-17/Th17/T regulatory cells (Treg) balance, and to summarize the development of IL-17-targeted therapies for autoimmune thyroid disease (AITD).

methodsA comprehensive literature review (up to 2025) was conducted, encompassing human studies, animal models, and pre-clinical investigations related to IL-17/Th17 biology in AITD.

resultsIL-17 levels are elevated in both untreated and intractable GD. IL-17/IL-17RA signalling enhances the expression of IL-6, chemokine CXC ligand 10, and intercellular cell adhesion molecule-1, thereby amplifying thyroid inflammation. The IL-23/IL-17 axis and Th17/Treg imbalance are strongly associated with thyroid-associated ophthalmopathy. Serum and tissue IL-17 concentrations correlate positively with TPOAb or TgAb titres and early fibrosis, while Th17 predominance precedes Th1-mediated tissue destruction. Excessive iodine intake further drives naïve Tregs toward Th17 differentiation. Shared TGF-β signalling drives the reciprocal development of Th17 and Treg cells, with retinoid-related orphan receptor gamma t and Forkhead box protein P3 acting as molecular switches. Disruption of this balance contributes to the progression of AITD. Several pre-clinical agents (JiaYanKangTai, Yanghe decoction, LY294002) have been found to ameliorate experimental autoimmune thyroiditis by inhibiting IL-17 signalling or restoring Th17/Treg equilibrium; however, clinical translation remains limited.

conclusionsIL-23/IL-17 axis and Th17/Treg imbalance are critical checkpoints in the AITD pathogenesis. IL-17 represents a promising, yet still experimental immunotherapeutic target, warranting rigorous clinical investigation.

Indexed as

Graves DiseaseHashimoto DiseaseInterleukin-17Th17 CellsAnimalsDisease Models, AnimalHumansSignal TransductionT-Lymphocytes, RegulatoryInterleukin-17Autoimmune thyroid diseasescytokineimmunotherapyinterleukin 17T helper cells 17

Identifiers

PMID41243116
PMCPMC12624951

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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.