Evidence map›Paper›PMID 26101460›Full record

ReviewMediators of inflammation2015

Harnessing the Therapeutic Potential of Th17 Cells.

Jonas Bystrom, Taher E Taher, M Sherwan Muhyaddin, Felix I Clanchy, Pamela Mangat, Ali S Jawad, Richard O Williams, Rizgar A Mageed

Open access · goldAbstract readReview
In one paragraph

Review in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.2field-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

19 citing papers in PubMed, 40 citations in OpenAlex.

  1. Potential Pathogens Associated with Colorectal Cancer.Current pharmaceutical biotechnology · 2025
    Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. The Mechanism ofThe Malaysian journal of medical sciences : MJMS · 2020
    Review
  8. Review
  9. Article
  10. Review
  11. The Interleukin-17 Family of Cytokines in Breast Cancer.International journal of molecular sciences · 2018
    Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

8 authors at 6 institutions in 2 countries.

Jonas BystromBone and Joint Research Unit, William Harvey Research Institute, Queen Mary University of London, London EC1M 6BQ, UK.
Taher E TaherBone and Joint Research Unit, William Harvey Research Institute, Queen Mary University of London, London EC1M 6BQ, UK.
M Sherwan MuhyaddinCollege of Pharmacy, Hawler Medical University, Erbil, Iraq.
Felix I ClanchyKennedy Institute of Rheumatology, University of Oxford, Oxford OX3 7FY, UK.
Pamela MangatDepartment of Rheumatology, Royal Free Hospital, London NW3 2GQ, UK.
Ali S JawadDepartment of Rheumatology, The Royal London Hospital, London E1 4DG, UK.
Richard O WilliamsKennedy Institute of Rheumatology, University of Oxford, Oxford OX3 7FY, UK.
Rizgar A MageedBone and Joint Research Unit, William Harvey Research Institute, Queen Mary University of London, London EC1M 6BQ, UK.
University of Oxford · GBWilliam Harvey Research Institute · GBHawler Medical University · IQQueen Mary University of London · GBRoyal London Hospital · GBUniversity College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Th17 cells provide protective immunity to infections by fungi and extracellular bacteria as well as cancer but are also involved in chronic inflammation. The cells were first identified by their ability to produce interleukin 17A (IL-17A) and, subsequently, associated with chronic inflammation and autoimmunity. Th17 cells have some gene profile similarity with stem cells and can remain dormant in mucosal tissues for long periods. Indeed, recent studies suggest that functionally distinct subsets of pro- and anti-inflammatory Th17 cells can interchange phenotype and functions. For development, Th17 cells require activation of the transcription factors STAT3 and RORγt while RUNX1, c-Maf, and Aiolos are involved in changes of phenotype/functions. Attempts to harness Th17 cells against pathogens and cancer using vaccination strategies are being explored. The cells gain protective abilities when induced to produce interferon γ (IFNγ). In addition, treatment with antibodies to IL-17 is effective in treating patients with psoriasis, psoriatic arthritis, and refectory rheumatoid arthritis. Moreover, since RORγt is a nuclear receptor, it is likely to be a potential future drug target for modulating Th17 functions. This review explores pathways through which Th17 subsets are induced, the molecular basis of their plasticity, and potential therapeutic strategies for their modulation in diseases.

Indexed as

Autoimmune DiseasesCell PlasticityHumansInterferon-gammaMycobacterium tuberculosisNeoplasmsPseudomonas aeruginosaStreptococcus pneumoniaeTh17 CellsVaccinationInterferon-gamma

Identifiers

PMID26101460
PMCPMC4460252
OpenAlexW1516709159

What OpenQuestion holds

Textmetadata
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.