Evidence map›Paper›PMID 24498362›Full record

ArticlePloS one2014

Prevention of allogeneic cardiac graft rejection by transfer of ex vivo expanded antigen-specific regulatory T-cells.

Fumika Takasato, Rimpei Morita, Takashi Schichita, Takashi Sekiya, Yasuhide Morikawa, Tatsuo Kuroda, Masanori Niimi, Akihiko Yoshimura

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
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  6. Engineering therapeutic T cells to suppress alloimmune responses using TCRs, CARs, or BARs.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2018
    Review
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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 4 institutions in 1 country.

Fumika TakasatoDepartment of Microbiology and Immunology, Keio University School of Medicine, Tokyo, Japan ; Department of Pediatric Surgery, Keio University School of Medicine, Tokyo, Japan ; Japan Science and Technology Agency, CREST, Tokyo, Japan.
Rimpei MoritaDepartment of Microbiology and Immunology, Keio University School of Medicine, Tokyo, Japan ; Japan Science and Technology Agency, CREST, Tokyo, Japan.
Takashi SchichitaDepartment of Microbiology and Immunology, Keio University School of Medicine, Tokyo, Japan ; Japan Science and Technology Agency, CREST, Tokyo, Japan.
Takashi SekiyaDepartment of Microbiology and Immunology, Keio University School of Medicine, Tokyo, Japan ; Japan Science and Technology Agency, CREST, Tokyo, Japan.
Yasuhide MorikawaDepartment of Pediatric Surgery, International University Medical Welfare Hospital, Nasushiobara, Tochigi, Japan.
Tatsuo KurodaDepartment of Pediatric Surgery, Keio University School of Medicine, Tokyo, Japan.
Masanori NiimiDepartment of Surgery, Teikyo University School of Medicine, Tokyo, Japan.
Akihiko YoshimuraDepartment of Microbiology and Immunology, Keio University School of Medicine, Tokyo, Japan ; Japan Science and Technology Agency, CREST, Tokyo, Japan.
Japan Science and Technology Agency · JPKeio University · JPInternational University of Health and Welfare · JPTeikyo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The rate of graft survival has dramatically increased using calcineurin inhibitors, however chronic graft rejection and risk of infection are difficult to manage. Induction of allograft-specific regulatory T-cells (Tregs) is considered an ideal way to achieve long-term tolerance for allografts. However, efficient in vitro methods for developing allograft-specific Tregs which is applicable to MHC full-mismatched cardiac transplant models have not been established. We compared antigen-nonspecific polyclonal-induced Tregs (iTregs) as well as antigen-specific iTregs and thymus-derived Tregs (nTregs) that were expanded via direct and indirect pathways. We found that iTregs induced via the indirect pathway had the greatest ability to prolong graft survival and suppress angiitis. Antigen-specific iTregs generated ex vivo via both direct and indirect pathways using dendritic cells from F1 mice also induced long-term engraftment without using MHC peptides. In antigen-specific Treg transferred models, activation of dendritic cells and allograft-specific CTL generation were suppressed. The present study demonstrated the potential of ex vivo antigen-specific Treg expansion for clinical cell-based therapeutic approaches to induce lifelong immunological tolerance for allogeneic cardiac transplants.

Indexed as

Heart TransplantationAdoptive TransferAnimalsAntigen PresentationDendritic CellsGraft RejectionGraft SurvivalGraft vs Host DiseaseMiceMice, Inbred BALB CMice, Inbred C57BLMice, Inbred CBAT-Lymphocytes, RegulatoryTransplantation, Homologous

Identifiers

PMID24498362
PMCPMC3912059
OpenAlexW2022103053

What OpenQuestion holds

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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.