Evidence map›Paper›PMID 24594640›Full record

ArticlePloS one2014

Ex vivo expanded human regulatory T cells delay islet allograft rejection via inhibiting islet-derived monocyte chemoattractant protein-1 production in CD34+ stem cells-reconstituted NOD-scid IL2rγnull mice.

Fang Xiao, Liang Ma, Min Zhao, Guocai Huang, Vincenzo Mirenda, Anthony Dorling, Robert Lechler, Giovanna Lombardi

Erratum issuedOpen 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. An erratum has been issued. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
7.0field-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

32 citing papers in PubMed, 57 citations in OpenAlex.

  1. Engineering hypoimmune stem cell-derived beta cells.Stem cell research & therapy · 2025
    Review
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  3. Immunosuppressant therapy averts rejection of allogeneic FKBP1A-disrupted CAR-T cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
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  13. Decreased interleukin-35 levels and CD4Archives of medical science : AMS · 2021
    Article
  14. TNature reviews. Immunology · 2020
    Review
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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Fang XiaoMedical Research Council (MRC) for Transplantation, King's College London, London, United Kingdom.
Liang MaMedical Research Council (MRC) for Transplantation, King's College London, London, United Kingdom.
Min ZhaoDepartment of Diabetes & Endocrinology, King's College London, London, United Kingdom.
Guocai HuangDepartment of Diabetes & Endocrinology, King's College London, London, United Kingdom.
Vincenzo MirendaMedical Research Council (MRC) for Transplantation, King's College London, London, United Kingdom.
Anthony DorlingMedical Research Council (MRC) for Transplantation, King's College London, London, United Kingdom.
Robert LechlerMedical Research Council (MRC) for Transplantation, King's College London, London, United Kingdom.
Giovanna LombardiMedical Research Council (MRC) for Transplantation, King's College London, London, United Kingdom.
King's College London · GBMedical Research Council · GB

Funding

British Heart Foundation RG/08/005/25303British Heart Foundation RG/13/12/30395Medical Research Council G0801965Medical Research Council MR/J006742/1
6 · The paper itself

Abstract

Type 1 diabetes mellitus (T1DM) is an autoimmune disease caused by immune-mediated destruction of insulin-secreting β cells of the pancreas. Near complete dependence on exogenous insulin makes T1DM very difficult to control, with the result that patients are exposed to high blood glucose and risk of diabetic complications and/or intermittent low blood glucose that can cause unconsciousness, fits and even death. Allograft transplantation of pancreatic islets restores normoglycemia with a low risk of surgical complications. However, although successful immediately after transplantation, islets are progressively lost, with most of the patients requiring exogenous insulin within 2 years post-transplant. Therefore, there is an urgent requirement for the development of new strategies to prevent islet rejection. In this study, we explored the importance of human regulatory T cells in the control of islets allograft rejection. We developed a pre-clinical model of human islet transplantation by reconstituting NOD-scid IL2rγnull mice with cord blood-derived human CD34+ stem cells and demonstrated that although the engrafted human immune system mediated the rejection of human islets, their survival was significantly prolonged following adoptive transfer of ex vivo expanded human Tregs. Mechanistically, Tregs inhibited the infiltration of innate immune cells and CD4+ T cells into the graft by down-regulating the islet graft-derived monocyte chemoattractant protein-1. Our findings might contribute to the development of clinical strategies for Treg therapy to control human islet rejection. We also show for the first time that CD34+ cells-reconstituted NOD-scid IL2rγnull mouse model could be beneficial for investigating human innate immunity in vivo.

Indexed as

AnimalsAntigens, CD34Chemokine CCL2Coculture TechniquesGraft RejectionHumansIn Vitro TechniquesIslets of Langerhans TransplantationMiceMice, Inbred NODMice, KnockoutMice, SCIDReceptors, Interleukin-2Stem CellsT-Lymphocytes, RegulatoryAntigens, CD34Chemokine CCL2Receptors, Interleukin-2

Identifiers

PMID24594640
PMCPMC3940883
OpenAlexW1975409023

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.