Evidence map›Paper›PMID 32397343›Full record

ReviewInternational journal of molecular sciences2020

The Role of TNFR2 and DR3 in the In Vivo Expansion of Tregs in T Cell Depleting Transplantation Regimens.

Jose-Ignacio Rodriguez-Barbosa, Pascal Schneider, Luis Graca, Leo Bühler, Jose-Antonio Perez-Simon, Maria-Luisa Del Rio

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. A TNF receptor 2 agonist ameliorates neuropathology and improves cognition in an Alzheimer's disease mouse model.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  8. Review
  9. Review
  10. 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

6 authors at 5 institutions in 3 countries.

Jose-Ignacio Rodriguez-BarbosaTransplantation Immunobiology, School of Biology and Biotechnology, Institute of Molecular Biology, Genomics and Proteomics, University of Leon, 24071 Leon, Spain.ORCID 0000-0001-7427-5654
Pascal SchneiderDepartment of Biochemistry, University of Lausanne, 1066 Epalinges, Switzerland.ORCID 0000-0003-0677-9409
Luis GracaSchool of Medicine, Institute of Molecular Medicine, University of Lisbon, Avenida Professor Egas Moniz, 1649-028 Lisbon, Portugal.
Leo BühlerFaculty of Science and Medicine, Section of Medicine, University of Fribourg, 1700 Fribourg, Switzerland.
Jose-Antonio Perez-SimonDepartment of Hematology, Institute of Biomedicine (IBIS/CSIC), University Hospital Virgen del Rocio, 41013 Sevilla, Spain.
Maria-Luisa Del RioTransplantation Immunobiology, School of Biology and Biotechnology, Institute of Molecular Biology, Genomics and Proteomics, University of Leon, 24071 Leon, Spain.ORCID 0000-0003-3710-2847
Universidad de León · ESInstituto de Biomedicina de Sevilla · ESUniversity of Fribourg · CHUniversity of Lausanne · CHUniversity of Lisbon · PT

Funding

Fondo de Investigaciones Sanitarias CB16/12/00480Fondo de Investigaciones Sanitarias PI13/00029Fondo de Investigaciones Sanitarias PI16/00002Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung 31003A-176526
6 · The paper itself

Abstract

Regulatory T cells (Tregs) are essential for the maintenance of tolerance to self and non-self through cell-intrinsic and cell-extrinsic mechanisms. Peripheral Tregs survival and clonal expansion largely depend on IL-2 and access to co-stimulatory signals such as CD28. Engagement of tumor necrosis factor receptor (TNFR) superfamily members, in particular TNFR2 and DR3, contribute to promote peripheral Tregs expansion and sustain their survival. This property can be leveraged to enhance tolerance to allogeneic transplants by tipping the balance of Tregs over conventional T cells during the course of immune reconstitution. This is of particular interest in peri-transplant tolerance induction protocols in which T cell depletion is applied to reduce the frequency of alloreactive T cells or in conditioning regimens that allow allogeneic bone marrow transplantation. These conditioning regimens are being implemented to limit long-term side effects of continuous immunosuppression and facilitate the establishment of a state of donor-specific tolerance. Lymphopenia-induced homeostatic proliferation in response to cytoreductive conditioning is a window of opportunity to enhance preferential expansion of Tregs during homeostatic proliferation that can be potentiated by agonist stimulation of TNFR.

Indexed as

Bone Marrow TransplantationLymphocyte DepletionAbataceptAdoptive TransferAllograftsAnimalsCell DifferentiationCell DivisionGraft RejectionHeart TransplantationHomeostasisHumansImmune ToleranceLymphocyte TransfusionLymphopeniaMiceAbataceptReceptors, Tumor Necrosis Factor, Member 25Receptors, Tumor Necrosis Factor, Type IITnfrsf1b protein, mouseTNFRSF25 protein, humanTnfrsf25 protein, mouseTumor Necrosis Factor-alphagraft rejectiongraft-versus-host diseasehomeostatic proliferationlymphopeniaregulatory T cellsTNF/TNF receptorstransplantation

Identifiers

PMID32397343
PMCPMC7247540
OpenAlexW3021350320

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.