Evidence map›Paper›PMID 38622133›Full record

ArticleNature communications2024

Donor regulatory T cells rapidly adapt to recipient tissues to control murine acute graft-versus-host disease.

David J Dittmar, Franziska Pielmeier, Nicholas Strieder, Alexander Fischer, Michael Herbst, Hanna Stanewsky, Niklas Wenzl, Eveline Röseler, Rüdiger Eder, Claudia Gebhard and 6 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Engineered CD40-biosensor-expressing Treg cells as a cell therapy approach for inflammatory diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. 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

16 authors at 3 institutions in 2 countries.

David J Dittmar *Department of Internal Medicine III, University Hospital Regensburg, 93053, Regensburg, Germany.ORCID http://orcid.org/0009-0000-3721-2590
Franziska Pielmeier *Department of Internal Medicine III, University Hospital Regensburg, 93053, Regensburg, Germany.
Nicholas StriederLeibniz Institute for Immunotherapy, 93053, Regensburg, Germany.ORCID http://orcid.org/0000-0003-1183-1099
Alexander FischerDepartment of Internal Medicine III, University Hospital Regensburg, 93053, Regensburg, Germany.ORCID http://orcid.org/0000-0001-8876-5566
Michael HerbstDepartment of Internal Medicine III, University Hospital Regensburg, 93053, Regensburg, Germany.ORCID http://orcid.org/0000-0001-9443-4093
Hanna StanewskyDepartment of Internal Medicine III, University Hospital Regensburg, 93053, Regensburg, Germany.
Niklas WenzlLeibniz Institute for Immunotherapy, 93053, Regensburg, Germany.
Eveline RöselerLeibniz Institute for Immunotherapy, 93053, Regensburg, Germany.
Rüdiger EderDepartment of Internal Medicine III, University Hospital Regensburg, 93053, Regensburg, Germany.
Claudia GebhardLeibniz Institute for Immunotherapy, 93053, Regensburg, Germany.
Lucia Schwarzfischer-PfeilschifterDepartment of Internal Medicine III, University Hospital Regensburg, 93053, Regensburg, Germany.
Christin AlbrechtDepartment of Internal Medicine III, University Hospital Regensburg, 93053, Regensburg, Germany.
Wolfgang HerrDepartment of Internal Medicine III, University Hospital Regensburg, 93053, Regensburg, Germany.
Matthias EdingerDepartment of Internal Medicine III, University Hospital Regensburg, 93053, Regensburg, Germany. matthias.edinger@ukr.de.ORCID http://orcid.org/0000-0003-2889-2533
Petra HoffmannDepartment of Internal Medicine III, University Hospital Regensburg, 93053, Regensburg, Germany. petra.hoffmann@ukr.de.ORCID http://orcid.org/0009-0003-3541-6196
Michael RehliDepartment of Internal Medicine III, University Hospital Regensburg, 93053, Regensburg, Germany. michael.rehli@ukr.de.ORCID http://orcid.org/0000-0003-3992-932X
University Hospital Regensburg · DELeibniz Association · DEUniversity of Zurich · CH

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) TRR221-B07
6 · The paper itself

Abstract

The adoptive transfer of regulatory T cells is a promising strategy to prevent graft-versus-host disease after allogeneic bone marrow transplantation. Here, we use a major histocompatibility complex-mismatched mouse model to follow the fate of in vitro expanded donor regulatory T cells upon migration to target organs. Employing comprehensive gene expression and repertoire profiling, we show that they retain their suppressive function and plasticity after transfer. Upon entering non-lymphoid tissues, donor regulatory T cells acquire organ-specific gene expression profiles resembling tissue-resident cells and activate hallmark suppressive and cytotoxic pathways, most evidently in the colon, when co-transplanted with graft-versus-host disease-inducing conventional T cells. Dominant T cell receptor clonotypes overlap between organs and across recipients and their relative abundance correlates with protection efficacy. Thus, this study reveals donor regulatory T cell selection and adaptation mechanisms in target organs and highlights protective features of Treg to guide the development of improved graft-versus-host disease prevention strategies.

Indexed as

Graft vs Host DiseaseT-Lymphocytes, RegulatoryAnimalsBone Marrow TransplantationMiceMice, Inbred C57BLTransplantation, Homologous

Identifiers

PMID38622133
PMCPMC11018811
OpenAlexW4394815629

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.