Evidence map›Paper›PMID 23234343›Full record

ArticleThyroid : official journal of the American Thyroid Association2013

Demonstration of innate immune responses in the thyroid gland: potential to sense danger and a possible trigger for autoimmune reactions.

Akira Kawashima, Kazuko Yamazaki, Takeshi Hara, Takeshi Akama, Aya Yoshihara, Mariko Sue, Kazunari Tanigawa, Huhehasi Wu, Yuko Ishido, Fumihiko Takeshita and 3 more

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In one paragraph

Article in Thyroid : official journal of the American Thyroid Association, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 2 pooled it
1.7field-weighted citation impact, top 17% 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

29 citing papers in PubMed, 2 syntheses or guidelines pooled it, 55 citations in OpenAlex.

  1. Pooled it
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  7. Review
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  12. Thyrotoxicosis occurrence in SARS-CoV-2 infection: A case report.Annals of medicine and surgery (2012) · 2022
    Article
  13. Review
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  15. Article
  16. Article
  17. Association of IL-1BioMed research international · 2021
    Article
  18. Article
  19. Article
  20. Innate Immune-Modulatory Activity ofFrontiers in endocrinology · 2020
    Article
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

13 authors at 4 institutions in 1 country.

Akira KawashimaLaboratory of Molecular Diagnostics, Department of Mycobacteriology, National Institute of Infectious Diseases, Tokyo, Japan.
Kazuko Yamazaki
Takeshi Hara
Takeshi Akama
Aya Yoshihara
Mariko Sue
Kazunari Tanigawa
Huhehasi Wu
Yuko Ishido
Fumihiko Takeshita
Norihisa Ishii
Kanji Sato
Koichi Suzuki
National Institute of Infectious Diseases · JPKanto Central Hospital · JPNational Institute of Biomedical Innovation, Health and Nutrition · JPTokyo Women's Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAutoimmune thyroid disease is an archetypal organ-specific autoimmune disorder that is characterized by the production of thyroid autoantibodies and lymphocytic infiltration into the thyroid. However, the underlying mechanisms by which specific thyroid antibodies are produced are largely unknown. Recent studies have shown that innate immune responses affect both the phenotype and the severity of autoimmune reactions. Moreover, it appears that even non-immune cells, including thyroid cells, have an ability to launch such responses. The aim of this study was to conduct a more detailed analysis of innate immune responses of the thyroid upon stimulation with various "non-self" and "self" factors that might contribute to the initiation of autoimmune reactions.

methodsWe used rat thyroid FRTL-5 cells, human thyroid cells, and mice to investigate the effects of various pathogen-associated molecular patterns (PAMPs), danger-associated molecular patterns (DAMPs), and iodide on gene expression and function that were related to innate immune responses.

resultsRT-PCR analysis showed that both rat and human thyroid cells expressed mRNAs for Toll-like receptors (TLRs) that sensed PAMPs. Stimulation of thyrocytes with TLR ligands resulted in activation of the interferon-beta (IFN-β) promoter and the nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB)-dependent promoter. As a result, pro-inflammatory cytokines, chemokines, and type I interferons were produced. Similar activation was observed when thyroid cells were stimulated with double-stranded DNA, one of the typical DAMPs. In addition to these PAMPs and DAMPs, treatment of thyroid cells with high concentrations of iodide increased mRNA expression of various cytokines.

conclusionWe show that thyroid cells express functional sensors for exogenous and endogenous dangers, and that they are capable of launching innate immune responses without the assistance of immune cells. Such responses may relate to the development of thyroiditis, which in turn may trigger autoimmune reactions.

Indexed as

AnimalsAutoimmune DiseasesAutoimmunityCell LineHumansImmunity, InnateInterferon-betaMiceRatsRNA, MessengerThyroid DiseasesThyroid GlandToll-Like ReceptorsInterferon-betaRNA, MessengerToll-Like Receptors

Identifiers

PMID23234343
PMCPMC3610444
OpenAlexW2090685556

What OpenQuestion holds

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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.