Evidence map›Paper›PMID 26450881›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2015

IL-7R signaling in regulatory T cells maintains peripheral and allograft tolerance in mice.

Mathias Schmaler, Maria A S Broggi, Nadège Lagarde, Benjamin F Stöcklin, Carolyn G King, Daniela Finke, Simona W Rossi

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Identification ofFrontiers in immunology · 2026
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  13. IL-7Rα on CD4Journal of neuroinflammation · 2024
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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

7 authors at 2 institutions in 1 country.

Mathias SchmalerDepartment of Biomedicine, Immunoregulation, University of Basel and University Hospital of Basel, Basel 4031, Switzerland; m.schmaler@unibas.ch simona.rossi@unibas.ch.
Maria A S BroggiDepartment of Biomedicine, Immunoregulation, University of Basel and University Hospital of Basel, Basel 4031, Switzerland;
Nadège LagardeDepartment of Biomedicine, Immunoregulation, University of Basel and University Hospital of Basel, Basel 4031, Switzerland;
Benjamin F StöcklinDepartment of Biomedicine, Immunoregulation, University of Basel and University Hospital of Basel, Basel 4031, Switzerland;
Carolyn G KingDepartment of Biomedicine, Transplantation Immunology and Nephrology, University of Basel and University Hospital of Basel, Basel 4031, Switzerland;
Daniela FinkeDepartment of Biomedicine, University of Basel and University Hospital of Basel, Basel 4058, Switzerland.
Simona W RossiDepartment of Biomedicine, Immunoregulation, University of Basel and University Hospital of Basel, Basel 4031, Switzerland; m.schmaler@unibas.ch simona.rossi@unibas.ch.
University Hospital of Basel · CHUniversity of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Foxp3(+)CD4(+) regulatory T cells (Treg) have a crucial role in controlling CD4(+) T-cell activation, proliferation, and effector function. However, the molecular mechanisms regulating Treg function remain poorly understood. Here we assessed the role of IL-7, a key cytokine regulating T-cell homeostasis, in suppressor capacity of Treg. Using a skin allograft model in which transplant acceptance is controlled by the number of transferred Treg, we find that Treg impair the proliferation of allogeneic CD4(+) T cells, decrease production of IFNγ by effector T cells, and prevent early and increase late IL-7 induction by lymph node stromal cells. Increased IL-7 availability enhanced Treg survival, stabilized Treg molecular signature, enhanced surface IL-2Rα expression, and improved IL-2 binding of Treg, which diminished proliferation of alloreactive CD4(+) T cells. Sequestration of IL-7 or impairment of IL-7R signaling after allograft transplantation abolished Treg-mediated tolerance by limiting their suppressive capacity. Aged Il7rα-ΔTreg mice displayed mild symptoms of autoimmunity correlating with impaired expansion of effector Treg in response to IL-2. Thus, IL-7R signaling on Treg supports the functional activity of effector Treg by increasing their IL-2 sensitivity in the lymph node during peripheral and allograft tolerance.

Indexed as

AnimalsDNA PrimersFlow CytometryHistological TechniquesInterleukin-2Lymph NodesMicePeripheral ToleranceReceptors, Interleukin-7Reverse Transcriptase Polymerase Chain ReactionSignal TransductionSkin TransplantationStatistics, NonparametricT-Lymphocytes, RegulatoryTransplantation ToleranceDNA PrimersInterleukin-2Receptors, Interleukin-7IL-2IL-7IL-7Rregulatory T cellskin transplantation

Identifiers

PMID26450881
PMCPMC4629352
OpenAlexW2216056178

What OpenQuestion holds

Textmetadata
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.