Evidence map›Paper›PMID 25790134›Full record

ArticlePathogens (Basel, Switzerland)2015

TLR-2 Signaling Promotes IL-17A Production in CD4+CD25+Foxp3+ Regulatory Cells during Oropharyngeal Candidiasis.

Natarajan Bhaskaran, Samuel Cohen, Yifan Zhang, Aaron Weinberg, Pushpa Pandiyan

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 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
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  17. Clinical & translational immunology · 2020
    Article
  18. Article
  19. The Gut-liver Axis in Immune Remodeling: New insight into Liver Diseases.International journal of biological sciences · 2020
    Review
  20. Article
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

5 authors at 1 institution in 1 country.

Natarajan BhaskaranDepartment of Biological Sciences, School of Dental Medicine, Case Western Reserve University, Cleveland, OH 44106, USA. nxb160@case.edu.
Samuel CohenDepartment of Biological Sciences, School of Dental Medicine, Case Western Reserve University, Cleveland, OH 44106, USA. shc30@case.edu.
Yifan ZhangDepartment of Biological Sciences, School of Dental Medicine, Case Western Reserve University, Cleveland, OH 44106, USA. ycz@case.edu.
Aaron WeinbergDepartment of Biological Sciences, School of Dental Medicine, Case Western Reserve University, Cleveland, OH 44106, USA. axw47@case.edu.
Pushpa PandiyanDepartment of Biological Sciences, School of Dental Medicine, Case Western Reserve University, Cleveland, OH 44106, USA. pxp226@case.edu.
Case Western Reserve University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies show that CD4+CD25+Foxp3+ regulatory cells (Tregs) produce effector cytokines under inflammatory conditions. However, the direct role of microbial agents that serve as toll-like receptor (TLR) ligands in the induction of effector cytokines in Tregs is less clear. Here we show that CD4+Foxp3+Tregs produce the effector cytokine IL-17A during oropharyngeal candidiasis (OPC) and inflammatory bowel disease in a TLR-2/Myd88 signaling dependent manner. TLR-2 ligands promote proliferation in Tregs in the presence and absence of TCR signals and inflammatory cytokines in vitro. The proliferation is directly dependent on TLR-2 expression in Tregs. Consistent with this, Tlr2-/- mice harbor fewer thymically derived Tregs and peripheral Tregs under homeostatic conditions in vivo. However, under Th17 inducing conditions, IL-6 and TLR-2 signaling both in Tregs as well as antigen presenting cells (APC) are critical for maximal ROR-γt and IL-17A up-regulation in Foxp3+ Tregs. The minimal and transient loss of Foxp3 expression and suppressive properties are due to the presence of IL-6 in the milieu, but not the direct effect of TLR-2 signaling in Tregs. Taken together, our data reveal that TLR-2 signaling promotes not only proliferation, but also IL-17A in Tregs, depending on the cytokine milieu. These IL-17A producing Tregs may be relevant in mucosal infections and inflammation.

Identifiers

PMID25790134
PMCPMC4384074
OpenAlexW2067428170

What OpenQuestion holds

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LicenceCC BY
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.