Evidence map›Paper›PMID 20674321›Full record

ReviewCurrent opinion in immunology2010

Inborn errors of mucocutaneous immunity to Candida albicans in humans: a role for IL-17 cytokines?

Anne Puel, Capucine Picard, Sophie Cypowyj, Desa Lilic, Laurent Abel, Jean-Laurent Casanova

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 2 pooled it
6.3field-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

80 citing papers in PubMed, 2 syntheses or guidelines pooled it, 137 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Article
  7. The ouroboros of autoimmunity.Nature immunology · 2024
    Review
  8. Review
  9. Article
  10. The Th17/IL-17 Axis and Host Defense Against Fungal Infections.The journal of allergy and clinical immunology. In practice · 2023
    Review
  11. Review
  12. Human autoantibodies underlying infectious diseases.The Journal of experimental medicine · 2022
    Article
  13. Article
  14. IntestinalFrontiers in microbiology · 2022
    Article
  15. Review
  16. Review
  17. Genetic susceptibility to fungal infection in children.Current opinion in pediatrics · 2020
    Review
  18. Review
  19. Review
  20. Review

20 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 5 institutions in 3 countries.

Anne PuelLaboratory of Human Genetics of Infectious Diseases, Necker Branch, Inserm U980, University Paris Descartes, Necker Medical School, Paris, France, EU. anne.puel@inserm.fr
Capucine Picard
Sophie Cypowyj
Desa Lilic
Laurent Abel
Jean-Laurent Casanova
Rockefeller University · USDélégation Paris 5 · FRInserm · FRNewcastle University · GBUniversité Paris Cité · FR

Funding

TRANSFORMING TRANSLATIONAL SCIENCE AND EDUCATION TO BENEFIT HUMAN HEALTHUL1RR024143 · NCRR · ROCKEFELLER UNIVERSITY · PI COLLER, BARRY · 2006 to 2011
$49.1M
NCRR NIH HHS 5UL1RR024143-03NCRR NIH HHS UL1 RR024143
6 · The paper itself

Abstract

The various clinical manifestations of chronic mucocutaneous candidiasis (CMC) often result from acquired T-cell immunodeficiencies. More rarely, CMC results from inborn errors of immunity, the recent dissection of which has shed light on the molecular mechanisms of mucocutaneous immunity to Candida albicans. CMC may accompany various other infectious diseases in patients with almost any broad and profound T-cell primary immunodeficiency. By contrast, CMC is one of the few key infections in patients with autosomal dominant hyper IgE syndrome (mutations in STAT3), and in rare patients with autosomal recessive predisposition to mucocutaneous and invasive fungal infections (mutation in CARD9). In patients with mutations in STAT3 and CARD9, the development of IL-17-producing T cells is impaired. Moreover, CMC is the principal, if not only, infection in patients with autosomal recessive autoimmune polyendocrinopathy syndrome-I (mutations in AIRE). Patients with this condition have high titers of neutralizing autoantibodies (auto-Abs) against the IL-17 cytokines IL-17A, IL-17F, and IL-22. Collectively, these data suggest that human IL-17A, IL-17F, and IL-22 are essential for mucocutaneous immunity to C. albicans. They also suggest that the distinct syndrome of isolated CMC, without auto-immunity or other infections, may be caused by inborn errors of IL-17 immunity.

Indexed as

Candida albicansCandidiasis, Chronic MucocutaneousGenetic Diseases, InbornHumansImmunityInterleukin-17T-Lymphocytes, Helper-InducerInterleukin-17

Identifiers

PMID20674321
PMCPMC3770911
OpenAlexW1968683200

What OpenQuestion holds

Textmetadata
LicenceTDM
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.