Evidence map›Paper›PMID 26213975›Full record

ArticlePathogens (Basel, Switzerland)2015

Neutrophils Do Not Express IL-17A in the Context of Acute Oropharyngeal Candidiasis.

Anna R Huppler, Akash H Verma, Heather R Conti, Sarah L Gaffen

Open access · goldAbstract read
In one paragraph

Article in Pathogens (Basel, Switzerland), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Immune Sensing ofJournal of fungi (Basel, Switzerland) · 2021
    Review
  6. Article
  7. Article
  8. Pathogens (Basel, Switzerland) · 2019
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. mTOR Mediates IL-23 Induction of Neutrophil IL-17 and IL-22 Production.Journal of immunology (Baltimore, Md. : 1950) · 2016
    Article
  18. Review
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

4 authors at 2 institutions in 1 country.

Anna R HupplerChildren's Hospital of Pittsburgh of UPMC, Department of Pediatrics, Pittsburgh, PA 15224, USA. ahuppler@mcw.edu.
Akash H VermaDepartment of Medicine, Division of Rheumatology & Clinical Immunology, University of Pittsburgh, BST S702, 200 Lothrop Street, Pittsburgh, PA 15261, USA. akash.verma@pitt.edu.
Heather R ContiDepartment of Medicine, Division of Rheumatology & Clinical Immunology, University of Pittsburgh, BST S702, 200 Lothrop Street, Pittsburgh, PA 15261, USA. hrc11@pitt.edu.
Sarah L GaffenDepartment of Medicine, Division of Rheumatology & Clinical Immunology, University of Pittsburgh, BST S702, 200 Lothrop Street, Pittsburgh, PA 15261, USA. sarah.gaffen@pitt.edu.
University of Pittsburgh · USMedical College of Wisconsin · US

Funding

Host and Fungal Regulation of Type 17 Immunity to Oral CandidiasisR37DE022550 · NIDCR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Sarah L Gaffen · 2017 to 2026
$5.6M
IL-17 Receptor Signaling in the Oral MucosaR01DE022550 · NIDCR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GAFFEN, SARAH L · 2012 to 2016
$2.1M
IL-23/STAT3-Driven Oral Immune Responses to Candida albicansR01DE023815 · NIDCR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GAFFEN, SARAH L · 2014 to 2018
$1.9M
Negative Control of IL-17R Signaling: Implications for Fungal ImmunityR01AI107825 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GAFFEN, SARAH L · 2014 to 2018
$1.9M
Salivary Gland IL-17R Signaling in Oral CandidiasisF32DE023293 · NIDCR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CONTI, HEATHER RAQUEL · 2012 to 2015
$168k
NIAID NIH HHS R01 AI107825NIDCR NIH HHS F32 DE023293NIDCR NIH HHS R01 DE022550NIDCR NIH HHS R01 DE023815NIDCR NIH HHS R37 DE022550
6 · The paper itself

Abstract

IL-17 protects against pathogens by acting on nonhematopoietic cells to induce neutrophil recruitment through upregulation of chemokines and G-CSF. IL-17- and Th17-deficient humans and mice are susceptible to mucosal Candida albicans infections, linked to impaired neutrophil responses. IL-17 production is traditionally associated with CD4+ Th17 cells. However, IL-17 is also expressed during innate responses to facilitate rapid pathogen clearance. Innate IL-17-expressing cells include various lymphocyte-type subsets, including ILC3, NKT, γδ-T and "natural" Th17 (nTh17) cells. Some reports suggest that neutrophils can express IL-17 during fungal infections. Here, we asked whether neutrophils serve as a source of IL-17 during acute oropharyngeal candidiasis (OPC) using an IL-17A fate-tracking reporter mouse. Mice were subjected to OPC for two days, and oral tissue was analyzed by flow cytometry. IL-17A was expressed by γδ-T cells and TCRβ+ natural Th17 (nTh17) cells, as recently reported. Although infiltrating neutrophils were recruited to the tongue following infection, they did not express the IL-17A reporter. Moreover, neutrophil-depleted mice exhibited normal transcription of both Il17a and downstream IL-17-dependent gene targets after Candida challenge. Thus, in acute OPC, neutrophils are not a measurable source of IL-17 production, nor are they necessary to trigger IL-17-dependent gene expression, although they are essential for ultimate pathogen control.

Indexed as

Candida albicansfungal infectionIL-17innate lymphocytemiceneutrophilsoral candidiasisTCRTh17γδ-T cell

Identifiers

PMID26213975
PMCPMC4584272
OpenAlexW1800708805

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.