Evidence map›Paper›PMID 25561237›Full record

ReviewInternational journal of molecular sciences2014

Cytokine-modulating strategies and newer cytokine targets for arthritis therapy.

Shivaprasad H Venkatesha, Steven Dudics, Bodhraj Acharya, Kamal D Moudgil

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
5.8field-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

44 citing papers in PubMed, 100 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Anti-inflammatory Effects of First-line Anti-arthritic Drugs on T-cell Activation.Anti-inflammatory & anti-allergy agents in medicinal chemistry · 2023
    Article
  14. Effects of nasal inflammation on the olfactory bulb.Journal of neuroinflammation · 2022
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. 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 1 institution in 1 country.

Shivaprasad H VenkateshaDepartment of Microbiology and Immunology, University of Maryland School of Medicine, 685 W. Baltimore Street, HSF-1, Suite 380, Baltimore, MD 21201, USA. hvshivaprasad@gmail.com.
Steven DudicsDepartment of Microbiology and Immunology, University of Maryland School of Medicine, 685 W. Baltimore Street, HSF-1, Suite 380, Baltimore, MD 21201, USA. sdudics1@gmail.com.
Bodhraj AcharyaDepartment of Microbiology and Immunology, University of Maryland School of Medicine, 685 W. Baltimore Street, HSF-1, Suite 380, Baltimore, MD 21201, USA. bacharya@som.umaryland.edu.
Kamal D MoudgilDepartment of Microbiology and Immunology, University of Maryland School of Medicine, 685 W. Baltimore Street, HSF-1, Suite 380, Baltimore, MD 21201, USA. kmoud001@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
NCCIH NIH HHS R01 AT004321NCCIH NIH HHS R01AT004321
6 · The paper itself

Abstract

Cytokines are the key mediators of inflammation in the course of autoimmune arthritis and other immune-mediated diseases. Uncontrolled production of the pro-inflammatory cytokines such as interferon-γ (IFN-γ), tumor necrosis factor α (TNFα), interleukin-6 (IL-6), and IL-17 can promote autoimmune pathology, whereas anti-inflammatory cytokines including IL-4, IL-10, and IL-27 can help control inflammation and tissue damage. The pro-inflammatory cytokines are the prime targets of the strategies to control rheumatoid arthritis (RA). For example, the neutralization of TNFα, either by engineered anti-cytokine antibodies or by soluble cytokine receptors as decoys, has proven successful in the treatment of RA. The activity of pro-inflammatory cytokines can also be downregulated either by using specific siRNA to inhibit the expression of a particular cytokine or by using small molecule inhibitors of cytokine signaling. Furthermore, the use of anti-inflammatory cytokines or cytokine antagonists delivered via gene therapy has proven to be an effective approach to regulate autoimmunity. Unexpectedly, under certain conditions, TNFα, IFN-γ, and few other cytokines can display anti-inflammatory activities. Increasing awareness of this phenomenon might help develop appropriate regimens to harness or avoid this effect. Furthermore, the relatively newer cytokines such as IL-32, IL-34 and IL-35 are being investigated for their potential role in the pathogenesis and treatment of arthritis.

Indexed as

Antibodies, MonoclonalArthritis, RheumatoidCytokinesGenetic TherapyHumansImmunosuppressive AgentsRNA InterferenceRNA, Small InterferingTumor Necrosis Factor-alphaAntibodies, MonoclonalCytokinesImmunosuppressive AgentsRNA, Small InterferingTumor Necrosis Factor-alpha

Identifiers

PMID25561237
PMCPMC4307281
OpenAlexW2007151534

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.