Evidence map›Paper›PMID 22838497›Full record

ReviewArthritis research & therapy2012

Mucocutaneous candidiasis: the IL-17 pathway and implications for targeted immunotherapy.

Anna R Huppler, Shrinivas Bishu, Sarah L Gaffen

Open access · goldAbstract readReview
In one paragraph

Review in Arthritis research & therapy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
5.7field-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

67 citing papers in PubMed, 142 citations in OpenAlex.

  1. Article
  2. Review
  3. mSphere · 2025
    Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Single-Nucleotide Polymorphisms of theInternational journal of molecular sciences · 2023
    Article
  10. Review
  11. Review
  12. Review of bimekizumab in the treatment of psoriasis.Human vaccines & immunotherapeutics · 2022
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Intestinal microbiota: a new force in cancer immunotherapy.Cell communication and signaling : CCS · 2020
    Review
  20. Article

7 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

3 authors at 3 institutions in 1 country.

Anna R Huppler
Shrinivas Bishu
Sarah L Gaffen
Children's Hospital of Pittsburgh · USRheumatology Consultants · USUniversity of Pittsburgh · US

Funding

Digestive Diseases Training ProgramT32DK063922 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ARTEEL, GAVIN E, YADAV, DHIRAJ · 2003 to 2022
$5.2M
IL-17 Receptor Signaling in the Oral MucosaR01DE022550 · NIDCR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GAFFEN, SARAH L · 2012 to 2016
$2.1M
Structure-Function Relationships in the IL-17 ReceptorR01AR054389 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GAFFEN, SARAH L · 2008 to 2012
$1.8M
NIAMS NIH HHS AR054389NIDCR NIH HHS DE022550NIDDK NIH HHS T32 DK063922
6 · The paper itself

Abstract

IL-17 and related cytokines are direct and indirect targets of selective immunosuppressive agents for the treatment of autoimmune diseases and other diseases of pathologic inflammation. Insights into the potential adverse effects of IL-17 blockade can be drawn from the experience of patients with deficiencies in the IL-17 pathway. A unifying theme of susceptibility to mucocutaneous candidiasis is seen in both mice and humans with a variety of genetic defects that converge on this pathway. Mucocutaneous candidiasis is a superficial infection of mucosal, nail or skin surfaces usually caused by the fungal pathogen Candida albicans. The morbidity of the disease includes significant pain, weight loss and secondary complications, including carcinoma and aneurysms. This review describes the known human diseases associated with chronic mucocutaneous candidiasis (CMC) as well as the known and proposed connections to IL-17 signaling. The human diseases include defects in IL-17 signaling due to autoantibodies (AIRE deficiency), receptor mutations (IL-17 receptor mutations) or mutations in the cytokine genes (IL17F and IL17A). Hyper-IgE syndrome is characterized by elevated serum IgE, dermatitis and recurrent infections, including CMC due to impaired generation of IL-17-producing Th17 cells. Mutations in STAT1, IL12B and IL12RB1 result in CMC secondary to decreased IL-17 production through different mechanisms. Dectin-1 defects and CARD9 defects result in susceptibility to C. albicans because of impaired host recognition of the pathogen and subsequent impaired generation of IL-17-producing T cells. Thus, recent discoveries of genetic predisposition to CMC have driven the recognition of the role of IL-17 in protection from mucosal fungal infection and should guide counseling and management of patients treated with pharmacologic IL-17 blockade.

Indexed as

AnimalsCandidiasis, Chronic MucocutaneousDrug Delivery SystemsHumansImmunotherapyInterleukin-17Interleukin-17

Identifiers

PMID22838497
PMCPMC3580547
OpenAlexW2113369941

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.