Evidence map›Paper›PMID 30155495›Full record

ReviewJournal of immunology research2018

The Anti-Inflammatory Mediator, Vasoactive Intestinal Peptide, Modulates the Differentiation and Function of Th Subsets in Rheumatoid Arthritis.

Raúl Villanueva-Romero, Irene Gutiérrez-Cañas, Mar Carrión, Selene Pérez-García, Iria V Seoane, Carmen Martínez, Rosa P Gomariz, Yasmina Juarranz

Open access · goldAbstract readReview
In one paragraph

Review in Journal of immunology research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
6.6field-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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Methyltransferase-like 3-mediated RNA NFrontiers in immunology · 2025
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Human CD4International journal of molecular sciences · 2022
    Article
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  12. 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

8 authors at 1 institution in 1 country.

Raúl Villanueva-RomeroDepartamento de Biología Celular, Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Universidad Complutense de Madrid, Madrid, Spain.
Irene Gutiérrez-CañasDepartamento de Biología Celular, Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Universidad Complutense de Madrid, Madrid, Spain.
Mar CarriónDepartamento de Biología Celular, Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Universidad Complutense de Madrid, Madrid, Spain.
Selene Pérez-GarcíaDepartamento de Biología Celular, Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Universidad Complutense de Madrid, Madrid, Spain.
Iria V SeoaneDepartamento de Biología Celular, Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Universidad Complutense de Madrid, Madrid, Spain.
Carmen MartínezDepartamento de Biología Celular, Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Universidad Complutense de Madrid, Madrid, Spain.
Rosa P GomarizDepartamento de Biología Celular, Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Universidad Complutense de Madrid, Madrid, Spain.
Yasmina JuarranzDepartamento de Biología Celular, Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Universidad Complutense de Madrid, Madrid, Spain.ORCID 0000-0001-5886-8273
Universidad Complutense de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic background, epigenetic modifications, and environmental factors trigger autoimmune response in rheumatoid arthritis (RA). Several pathogenic infections have been related to the onset of RA and may cause an inadequate immunological tolerance towards critical self-antigens leading to chronic joint inflammation and an imbalance between different T helper (Th) subsets. Vasoactive intestinal peptide (VIP) is a mediator that modulates all the stages comprised between the arrival of pathogens and Th cell differentiation in RA through its known anti-inflammatory and immunomodulatory actions. This "neuroimmunopeptide" modulates the pathogenic activity of diverse cell subpopulations involved in RA as lymphocytes, fibroblast-like synoviocytes (FLS), or macrophages. In addition, VIP decreases the expression of pattern recognition receptor (PRR) such as toll-like receptors (TLRs) in FLS from RA patients. These receptors act as sensors of pathogen-associated molecular pattern (PAMP) and damage-associated molecular pattern (DAMP) connecting the innate and adaptive immune system. Moreover, VIP modulates the imbalance between Th subsets in RA, decreasing pathogenic Th1 and Th17 subsets and favoring Th2 or Treg profile during the differentiation/polarization of naïve or memory Th cells. Finally, VIP regulates the plasticity between theses subsets. In this review, we provide an overview of VIP effects on the aforementioned features of RA pathology.

Indexed as

AnimalsAnti-Inflammatory AgentsArthritis, RheumatoidCell DifferentiationHumansImmunomodulationLymphocyte ActivationT-Lymphocytes, Helper-InducerT-Lymphocyte SubsetsVasoactive Intestinal PeptideAnti-Inflammatory AgentsVasoactive Intestinal Peptide

Identifiers

PMID30155495
PMCPMC6092975
OpenAlexW2886551420

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.