Evidence map›Paper›PMID 23026768›Full record

ReviewCurrent opinion in allergy and clinical immunology2012

Inborn errors of human IL-17 immunity underlie chronic mucocutaneous candidiasis.

Anne Puel, Sophie Cypowyj, László Maródi, Laurent Abel, Capucine Picard, Jean-Laurent Casanova

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in allergy and clinical immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 166 papers.

0numbers the graph read from it
0cells of the map it votes in
166citing papers in PubMed
9.2field-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

166 citing papers in PubMed, 314 citations in OpenAlex.

  1. Trial
  2. Article
  3. Decreased IL-17-producing TThe journal of allergy and clinical immunology. Global · 2026
    Article
  4. Review
  5. The pathogenicity and future treatment strategies ofFrontiers in cellular and infection microbiology · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Human immunity to fungal infections.The Journal of experimental medicine · 2025
    Review
  10. The monogenic landscape of human infectious diseases.The Journal of allergy and clinical immunology · 2025
    Review
  11. Article
  12. Role ofWorld journal of gastroenterology · 2024
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Helper T cell immunity in humans with inherited CD4 deficiency.The Journal of experimental medicine · 2024
    Article
  19. Article
  20. Review

106 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

6 authors at 3 institutions in 3 countries.

Anne PuelLaboratory of Human Genetics of Infectious Diseases, Necker Branch, Inserm U980 and University Paris Descartes, Necker Medical School, Paris Sorbonne Cité, Paris, France.
Sophie Cypowyj
László Maródi
Laurent Abel
Capucine Picard
Jean-Laurent Casanova
Rockefeller University · USUniversité Paris Cité · FRUniversity of Debrecen · HU

Funding

Transforming Translational Science and Education to Benefit Human HealthUL1TR000043 · NCATS · ROCKEFELLER UNIVERSITY · PI COLLER, BARRY · 2012 to 2015
$26.8M
NCATS NIH HHS 8UL1TR000043,NCATS NIH HHS UL1 TR000043
6 · The paper itself

Abstract

purpose of reviewChronic mucocutaneous candidiasis (CMC) is characterized by recurrent or persistent symptomatic infection of the nails, skin and mucosae mostly by Candida albicans. CMC is common in patients with profound primary T-cell immunodeficiency, who often display multiple infectious and autoimmune diseases. Patients with syndromic CMC, including autosomal dominant hyper IgE syndrome (AD-HIES) and autosomal recessive autoimmune polyendocrinopathy syndrome type I (APS-I), display fewer other infections. Patients with isolated CMC (CMCD) rarely display any other severe disease. We review here recent progress in the genetic dissection of these three types of inherited CMC. RECENT

findingsLow IL-17 T-cell proportions were reported in patients with AD-HIES bearing heterozygous STAT3 mutations, prone to CMC and staphylococcal diseases, and in a kindred with autosomal recessive CARD9 deficiency, prone to CMC and other fungal infections. High levels of neutralizing autoantibodies against IL-17 cytokines were documented in patients with APS-I presenting with CMC as their only infectious disease. The first three genetic causes of CMCD were then reported: autosomal recessive IL-17RA and autosomal dominant IL-17F deficiencies and autosomal dominant STAT1 gain-of-function, impairing IL-17-producing T-cell development. SUMMARY: Inborn errors of human IL-17 immunity underlie CMC. Impaired IL-17 immunity may therefore account for CMC in other settings, including patients with acquired immunodeficiency.

Indexed as

Candida albicansCandidiasis, Chronic MucocutaneousHumansInterleukin-17Job SyndromePolyendocrinopathies, AutoimmuneReceptors, Interleukin-17STAT Transcription FactorsIL17RA protein, humanInterleukin-17Receptors, Interleukin-17STAT Transcription Factors

Identifiers

PMID23026768
PMCPMC3538358
OpenAlexW2071504008

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.