Evidence map›Paper›PMID 27602020›Full record

ReviewFrontiers in endocrinology2016

Thyrotropin Receptor Epitope and Human Leukocyte Antigen in Graves' Disease.

Hidefumi Inaba, Leslie J De Groot, Takashi Akamizu

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.0field-weighted citation impact, top 14% of its field
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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. The role of autophagy in Graves disease: knowns and unknowns.Frontiers in cell and developmental biology · 2024
    Review
  6. Characterizing the Interplay of Lymphocytes in Graves' Disease.International journal of molecular sciences · 2023
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Graves' Orbitopathy: Report of 82 cases.La Tunisie medicale · 2021
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review
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

3 authors at 2 institutions in 2 countries.

Hidefumi InabaThe First Department of Medicine, Wakayama Medical University , Wakayama , Japan.
Leslie J De GrootDepartment of Cellular and Molecular Biology, University of Rhode Island , Providence, RI , USA.
Takashi AkamizuThe First Department of Medicine, Wakayama Medical University , Wakayama , Japan.
Wakayama Medical University · JPProvidence College · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Graves' disease (GD) is an organ-specific autoimmune disease, and thyrotropin (TSH) receptor (TSHR) is a major autoantigen in this condition. Since the extracellular domain of human TSHR (TSHR-ECD) is shed into the circulation, TSHR-ECD is a preferentially immunogenic portion of TSHR. Both genetic factors and environmental factors contribute to development of GD. Inheritance of human leukocyte antigen (HLA) genes, especially HLA-DR3, is associated with GD. TSHR-ECD protein is endocytosed into antigen-presenting cells (APCs), and processed to TSHR-ECD peptides. These peptide epitopes bind to HLA-class II molecules, and subsequently the complex of HLA-class II and TSHR-ECD epitope is presented to CD4+ T cells. The activated CD4+ T cells secrete cytokines/chemokines that stimulate B-cells to produce TSAb, and in turn hyperthyroidism occurs. Numerous studies have been done to identify T- and B-cell epitopes in TSHR-ECD, including (1) in silico, (2) in vitro, (3) in vivo, and (4) clinical experiments. Murine models of GD and HLA-transgenic mice have played a pivotal role in elucidating the immunological mechanisms. To date, linear or conformational epitopes of TSHR-ECD, as well as the molecular structure of the epitope-binding groove in HLA-DR, were reported to be related to the pathogenesis in GD. Dysfunction of central tolerance in the thymus, or in peripheral tolerance, such as regulatory T cells, could allow development of GD. Novel treatments using TSHR antagonists or mutated TSHR peptides have been reported to be effective. We review and update the role of immunogenic TSHR epitopes and HLA in GD, and offer perspectives on TSHR epitope specific treatments.

Indexed as

anti-TSHR-antibodyepitopeGraves’ diseaseHLATSH receptor

Identifiers

PMID27602020
PMCPMC4994058
OpenAlexW2509306558

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.