Evidence map›Paper›PMID 26064907›Full record

ReviewBioMed research international2015

T Helper 17/Regulatory T Cell Balance and Experimental Models of Peritoneal Dialysis-Induced Damage.

Georgios Liappas, Guadalupe Tirma Gónzalez-Mateo, Pedro Majano, José Antonio Sánchez-Tomero, Marta Ruiz-Ortega, Raquel Rodrigues Díez, Pilar Martín, Raquel Sanchez-Díaz, Rafael Selgas, Manuel López-Cabrera and 1 more

Erratum issuedOpen access · hybridAbstract readReview
In one paragraph

Review in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 23% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 5 institutions in 1 country.

Georgios LiappasDepartment of Immunology, Centro de Biología Molecular Severo Ochoa (CBM), Consejo Superior de Investigaciones Científicas (CSIC), 28049 Madrid, Spain ; Department of Nephrology, Instituto de Investigación del Hospital Universitario La Paz (IdiPAZ), 28046 Madrid, Spain.
Guadalupe Tirma Gónzalez-MateoDepartment of Immunology, Centro de Biología Molecular Severo Ochoa (CBM), Consejo Superior de Investigaciones Científicas (CSIC), 28049 Madrid, Spain ; Department of Nephrology, Instituto de Investigación del Hospital Universitario La Paz (IdiPAZ), 28046 Madrid, Spain.
Pedro MajanoDepartment of Molecular Biology, Instituto de La Princesa (IP), 28006 Madrid, Spain.
José Antonio Sánchez-TomeroNephrology Service, Hospital Universitario de La Princesa (IP), 28006 Madrid, Spain.
Marta Ruiz-OrtegaLaboratory of Cellular Biology and Rare Diseases, Fundación Jiménez Díaz, Universidad Autónoma de Madrid (UAM), 28040 Madrid, Spain.
Raquel Rodrigues DíezLaboratory of Cellular Biology and Rare Diseases, Fundación Jiménez Díaz, Universidad Autónoma de Madrid (UAM), 28040 Madrid, Spain.ORCID 0000-0002-6348-1505
Pilar MartínDepartment of Molecular and Vascular Inflammation, Centro Nacional de Investigaciones Cardiovasculares (CNIC), 28029 Madrid, Spain.
Raquel Sanchez-DíazDepartment of Molecular and Vascular Inflammation, Centro Nacional de Investigaciones Cardiovasculares (CNIC), 28029 Madrid, Spain.
Rafael SelgasDepartment of Nephrology, Instituto de Investigación del Hospital Universitario La Paz (IdiPAZ), 28046 Madrid, Spain.
Manuel López-CabreraDepartment of Immunology, Centro de Biología Molecular Severo Ochoa (CBM), Consejo Superior de Investigaciones Científicas (CSIC), 28049 Madrid, Spain.
Abelardo Aguilera PeraltaDepartment of Molecular Biology, Instituto de La Princesa (IP), 28006 Madrid, Spain.
Consejo Superior de Investigaciones Científicas · ESHospital Universitario de La Princesa · ESSpanish National Centre for Cardiovascular Research · ESUniversidad Autónoma de Madrid · ESHospital Universitario La Paz · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibrosis is a general complication in many diseases. It is the main complication during peritoneal dialysis (PD) treatment, a therapy for renal failure disease. Local inflammation and mesothelial to mesenchymal transition (MMT) are well known key phenomena in peritoneal damage during PD. New data suggest that, in the peritoneal cavity, inflammatory changes may be regulated at least in part by a delicate balance between T helper 17 and regulatory T cells. This paper briefly reviews the implication of the Th17/Treg-axis in fibrotic diseases. Moreover, it compares current evidences described in PD animal experimental models, indicating a loss of Th17/Treg balance (Th17 predominance) leading to peritoneal damage during PD. In addition, considering the new clinical and animal experimental data, new therapeutic strategies to reduce the Th17 response and increase the regulatory T response are proposed. Thus, future goals should be to develop new clinical biomarkers to reverse this immune misbalance and reduce peritoneal fibrosis in PD.

Indexed as

AnimalsDisease Models, AnimalFibrosisHumansInflammationPeritoneal DialysisPeritoneumTh17 CellsT-Lymphocytes, Regulatory

Identifiers

PMID26064907
PMCPMC4433660
OpenAlexW2118214854

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.