Evidence map›Paper›PMID 23379432›Full record

ArticleClinical and experimental immunology2013

Anti-cytokine autoantibodies suggest pathogenetic links with autoimmune regulator deficiency in humans and mice.

J Kärner, A Meager, M Laan, J Maslovskaja, M Pihlap, A Remm, E Juronen, A S B Wolff, E S Husebye, K T Podkrajšek and 5 more

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

32 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
  2. Article
  3. Sterile production of interferons in the thymus.Journal of immunology (Baltimore, Md. : 1950) · 2025
    Review
  4. Article
  5. Review
  6. Anticytokine Autoantibodies in Infectious Diseases: A Practical Overview.International journal of molecular sciences · 2023
    Review
  7. Autoantibodies Neutralizing Type III Interferons Are Uncommon in Patients with Severe Coronavirus Disease 2019 Pneumonia.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2023
    Article
  8. IL-34 deficiency impairs FOXP3Clinical and translational medicine · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Observational
  18. Article
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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 5 institutions in 4 countries.

J KärnerMolecular Pathology Group, University of Tartu, Tartu, Estonia.
A Meager
M Laan
J Maslovskaja
M Pihlap
A Remm
E Juronen
A S B Wolff
E S Husebye
K T Podkrajšek
N Bratanic
T Battelino
N Willcox
P Peterson
K Kisand
University of Tartu · EELjubljana University Medical Centre · SIUniversity of Bergen · NONational Institute for Biological Standards and Control · GBUniversity of Oxford · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoimmune polyendocrinopathy candidiasis ectodermal dystrophy (APECED) is a recessive disorder resulting from mutations in the autoimmune regulator (AIRE). The patients' autoantibodies recognize not only multiple organ-specific targets, but also many type I interferons (IFNs) and most T helper type 17 (Th17) cell-associated cytokines, whose biological actions they neutralize in vitro. These anti-cytokine autoantibodies are highly disease-specific: otherwise, they have been found only in patients with thymomas, tumours of thymic epithelial cells that fail to express AIRE. Moreover, autoantibodies against Th17 cell-associated cytokines correlate with chronic mucocutaneous candidiasis in both syndromes. Here, we demonstrate that the immunoglobulin (Ig)Gs but not the IgAs in APECED sera are responsible for neutralizing IFN-ω, IFN-α2a, interleukin (IL)-17A and IL-22. Their dominant subclasses proved to be IgG1 and, surprisingly, IgG4 without IgE, possibly implicating regulatory T cell responses and/or epithelia in their initiation in these AIRE-deficiency states. The epitopes on IL-22 and IFN-α2a appeared mainly conformational. We also found mainly IgG1 neutralizing autoantibodies to IL-17A in aged AIRE-deficient BALB/c mice - the first report of any target shared by these human and murine AIRE-deficiency states. We conclude that autoimmunization against cytokines in AIRE deficiency is not simply a mere side effect of chronic mucosal Candida infection, but appears to be related more closely to disease initiation.

Indexed as

AIRE ProteinAnimalsAutoantibodiesCytokinesHumansImmunodominant EpitopesImmunoglobulin GInterferon-alphaInterleukin-17Interleukin-22InterleukinsMiceMice, Inbred BALB CMice, Inbred C57BLPolyendocrinopathies, AutoimmuneTranscription FactorsAIRE ProteinAutoantibodiesCytokinesIL17A protein, humanImmunodominant EpitopesImmunoglobulin GInterferon-alphaInterleukin-17Interleukin-22InterleukinsTranscription Factors

Identifiers

PMID23379432
PMCPMC3569533
OpenAlexW1526946356

What OpenQuestion holds

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Registered trials

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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.