Evidence map›Paper›PMID 25595306›Full record

ArticleCytokine2015

Involvement of the IL-23/IL-17 axis and the Th17/Treg balance in the pathogenesis and control of autoimmune arthritis.

Brian Astry, Shivaprasad H Venkatesha, Kamal D Moudgil

Abstract read
In one paragraph

Article in Cytokine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
4.2field-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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Review
  5. Cytokines Associated with Activation of CD4International journal of molecular sciences · 2026
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
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  13. Article
  14. Article
  15. The IL-17 family in diseases: from bench to bedside.Signal transduction and targeted therapy · 2023
    Review
  16. The star target in SLE: IL-17.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Review
  17. Article
  18. Review
  19. Article
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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 1 institution in 1 country.

Brian AstryDepartment of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD 21201, United States.
Shivaprasad H VenkateshaDepartment of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD 21201, United States.
Kamal D MoudgilDepartment of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD 21201, United States. Electronic address: kmoudgil@som.umaryland.edu.
University of Maryland, Baltimore · US

Funding

Immune Modulation of Autoimmunity by Herbal ProductsR01AT004321 · NCCIH · UNIVERSITY OF MARYLAND BALTIMORE · PI MOUDGIL, KAMAL D · 2009 to 2012
$1.5M
Immune mechanisms of CAM intervention in autoimmunityF31AT007278 · NCCIH · UNIVERSITY OF MARYLAND BALTIMORE · PI ASTRY, BRIAN CALVIN · 2012 to 2013
$88k
NCCIH NIH HHS F31 AT007278NCCIH NIH HHS R01 AT004321
6 · The paper itself

Abstract

The T helper (Th) cell subsets are characterized by the type of cytokines produced and the master transcription factor expressed. Th1 cells participate in cell-mediated immunity, whereas Th2 cells promote humoral immunity. Furthermore, the two subsets can control each other. Thereby, Th1-Th2 balance offered a key paradigm in understanding the induction and regulation of immune pathology in autoimmune and other diseases. However, over the past decade, Th17 cells producing interleukin-17 (IL-17) have emerged as the major pathogenic T cell subset in many pathological conditions that were previously attributed to Th1 cells. In addition, the role of CD4+CD25+T regulatory cells (Treg) in controlling the activity of Th17 and other T cell subsets has increasingly been realized. Thereby, examination of the Th17/Treg balance in the course of autoimmune diseases has significantly advanced our understanding of the pathogenesis of these disorders. The differentiation of Th17 and Treg cells from naïve T cells is inter-related and controlled in part by the cytokine milieu. For example, transforming growth factor β (TGFβ) is required for Treg induction, whereas the same cytokine in the presence of IL-6 (or IL-1) promotes the differentiation of Th17. Furthermore, IL-23 plays a role in the maintenance of Th17. Accordingly, novel therapeutic approaches are being developed to target IL-23/IL-17 as well as to modulate the Th17/Treg balance in favor of immune regulation to control autoimmunity.

Indexed as

AnimalsArthritisArthritis, ExperimentalArthritis, RheumatoidAutoimmune DiseasesHumansInterleukin-17Interleukin-23Th17 CellsTh1-Th2 BalanceT-Lymphocytes, RegulatoryIL17A protein, humanInterleukin-17Interleukin-23ArthritisInterleukin-17Interleukin-23Regulatory T cellT helper 17

Identifiers

PMID25595306
PMCPMC4457562
OpenAlexW2016225102

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.