Evidence map›Paper›PMID 25480564›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

Th1/Th17 plasticity is a marker of advanced β cell autoimmunity and impaired glucose tolerance in humans.

Linnea Reinert-Hartwall, Jarno Honkanen, Harri M Salo, Janne K Nieminen, Kristiina Luopajärvi, Taina Härkönen, Riitta Veijola, Olli Simell, Jorma Ilonen, Aleksandr Peet and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 2 pooled it
7.0field-weighted citation impact, top 3% 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

51 citing papers in PubMed, 2 syntheses or guidelines pooled it, 73 citations in OpenAlex.

  1. Pooled it
  2. Sarcoidosis as an Autoimmune Disease.Frontiers in immunology · 2019
    Pooled it
  3. Trial
  4. Trial
  5. Review
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  9. Article
  10. Article
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  13. Article
  14. TNature immunology · 2023
    Review
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  17. Article
  18. CD4International journal of molecular sciences · 2021
    Review
  19. 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

15 authors at 8 institutions in 5 countries.

Linnea Reinert-HartwallDepartment of Vaccination and Immune Protection, National Institute for Health and Welfare, 00271 Helsinki, Finland;
Jarno HonkanenDepartment of Vaccination and Immune Protection, National Institute for Health and Welfare, 00271 Helsinki, Finland;
Harri M SaloDepartment of Vaccination and Immune Protection, National Institute for Health and Welfare, 00271 Helsinki, Finland;
Janne K NieminenDepartment of Vaccination and Immune Protection, National Institute for Health and Welfare, 00271 Helsinki, Finland;
Kristiina LuopajärviDepartment of Vaccination and Immune Protection, National Institute for Health and Welfare, 00271 Helsinki, Finland; Children's Hospital, University of Helsinki and Helsinki University Central Hospital, 00281 Helsinki, Finland;
Taina HärkönenChildren's Hospital, University of Helsinki and Helsinki University Central Hospital, 00281 Helsinki, Finland;
Riitta VeijolaDepartment of Pediatrics, Medical Research Center, Oulu University Hospital and University of Oulu, 90014 Oulu, Finland;
Olli SimellDepartment of Pediatrics, University of Turku, 20520 Turku, Finland;
Jorma IlonenImmunogenetics Laboratory, University of Turku, 20520 Turku, Finland; Department of Clinical Microbiology, University of Eastern Finland, 70211 Kuopio, Finland;
Aleksandr PeetDepartment of Pediatrics, University of Tartu and Children's Clinic of Tartu University Hospital, Tartu 51014, Estonia;
Vallo TillmannDepartment of Pediatrics, University of Tartu and Children's Clinic of Tartu University Hospital, Tartu 51014, Estonia;
Mikael KnipChildren's Hospital, University of Helsinki and Helsinki University Central Hospital, 00281 Helsinki, Finland; Folkhälsan Research Center, 00290 Helsinki, Finland; Diabetes and Obesity Research Program, University of Helsinki, 00290 Helsinki, Finland; Department of Pediatrics, Tampere University Hospital, 33521 Tampere, Finland; and.
Outi VaaralaChildren's Hospital, University of Helsinki and Helsinki University Central Hospital, 00281 Helsinki, Finland; Respiratory, Inflammatory and Autoimmune Diseases, Innovative Medicine, AstraZeneca, 43183 Mölndal, Sweden outi.vaarala@helsinki.fi.
DIABIMMUNE Study Group
DIABIMMUNE Study Group
University of Helsinki · FIFinnish Institute for Health and Welfare · FITartu University Hospital · EEUniversity of Turku · FIHelsinki University Hospital · FIOulu University Hospital · FIAstraZeneca (United Kingdom) · GBNational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Upregulation of IL-17 immunity and detrimental effects of IL-17 on human islets have been implicated in human type 1 diabetes. In animal models, the plasticity of Th1/Th17 cells contributes to the development of autoimmune diabetes. In this study, we demonstrate that the upregulation of the IL-17 pathway and Th1/Th17 plasticity in peripheral blood are markers of advanced β cell autoimmunity and impaired β cell function in human type 1 diabetes. Activated Th17 immunity was observed in the late stage of preclinical diabetes in children with β cell autoimmunity and impaired glucose tolerance, but not in children with early β cell autoimmunity. We found an increased ratio of IFN-γ/IL-17 expression in Th17 cells in children with advanced β cell autoimmunity, which correlated with HbA1c and plasma glucose concentrations in an oral glucose tolerance test, and thus impaired β cell function. Low expression of Helios was seen in Th17 cells, suggesting that Th1/Th17 cells are not converted thymus-derived regulatory T cells. Our results suggest that the development of Th1/Th17 plasticity may serve as a biomarker of disease progression from β cell autoantibody positivity to type 1 diabetes. These data in human type 1 diabetes emphasize the role of Th1/Th17 plasticity as a potential contributor to tissue destruction in autoimmune conditions.

Indexed as

AutoantibodiesAutoimmunityBiomarkersCells, CulturedChildChild, PreschoolDiabetes Mellitus, Type 1Disease ProgressionFemaleGlucose IntoleranceHumansIkaros Transcription FactorInsulin-Secreting CellsInterferon-gammaInterleukin-17Interleukin-9AutoantibodiesBiomarkersIkaros Transcription FactorIKZF2 protein, humanIL9 protein, humanInterferon-gammaInterleukin-17Interleukin-9

Identifiers

PMID25480564
PMCPMC4273995
OpenAlexW1906467669

What OpenQuestion holds

Textmetadata
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.