Evidence map›Paper›PMID 34981746›Full record

ReviewEuropean thyroid journal2022

Cellular and molecular basis of thyroid autoimmunity.

Joanna Bogusławska, Marlena Godlewska, Ewa Gajda, Agnieszka Piekiełko-Witkowska

Open access · diamondAbstract readReview
In one paragraph

Review in European thyroid journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 5 pooled it
14.4field-weighted citation impact, top 1% 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

87 citing papers in PubMed, 5 syntheses or guidelines pooled it, 106 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Salivary Alterations in Autoimmune Thyroid Diseases: A Systematic Review.International journal of environmental research and public health · 2023
    Pooled it
  4. Pooled it
  5. Pooled it
  6. Trial
  7. Article
  8. Association ofBiomedicines · 2026
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Transcriptomic and Neuroimaging Decoding of Brain-Immune Crosstalk in Thyroid Eye Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  17. Article
  18. Review
  19. Review
  20. Article

27 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Joanna BogusławskaCentre of Postgraduate Medical Education, Department of Biochemistry and Molecular Biology, Warsaw, Poland.
Marlena GodlewskaCentre of Postgraduate Medical Education, Department of Biochemistry and Molecular Biology, Warsaw, Poland.
Ewa GajdaCentre of Postgraduate Medical Education, Department of Biochemistry and Molecular Biology, Warsaw, Poland.
Agnieszka Piekiełko-WitkowskaCentre of Postgraduate Medical Education, Department of Biochemistry and Molecular Biology, Warsaw, Poland.
Postgraduate School of Molecular Medicine · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoimmune thyroid disease (AITD) is the most common human autoimmune disease. The two major clinical manifestations of AITD are Graves' disease and Hashimoto's thyroiditis (HT). AITD is characterized by lymphocytic infiltration of the thyroid gland, leading either to follicular cell damage, thyroid gland destruction, and development of hypothyroidism (in HT) or thyroid hyperplasia, induced by thyroid antibodies which activate thyrotropin receptor (TSHR) on thyrocytes, leading to hyperthyroidism. The aim of this review is to present up-to-date picture of the molecular and cellular mechanisms that underlie the pathology of AITD. Based on studies involving patients, animal AITD models, and thyroid cell lines, we discuss the key events leading to the loss of immune tolerance to thyroid autoantigens as well as the signaling cascades leading to the destruction of thyroid gland. Special focus is given on the interplay between the environmental and genetic factors, as well as ncRNAs and microbiome contributing to AITD development. In particular, we describe mechanistic models by which SNPs in genes involved in immune regulation and thyroid function, such as CD40, TSHR, FLT3, and PTPN22, underlie AITD predisposition. The clinical significance of novel diagnostic and prognostic biomarkers based on ncRNAs and microbiome composition is also underscored. Finally, we discuss the possible significance of probiotic supplementation on thyroid function in AITD.

Indexed as

AITDautoimmune thyroid diseasecircRNAsGraves’ diseaseHashimoto’s thyroiditislncRNAsmicrobiomemiRNAsnon-coding RNAsthyroid antigensthyroid autoimmunity

Identifiers

PMID34981746
PMCPMC9142813
OpenAlexW3209338751

What OpenQuestion holds

Textmetadata
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.