Evidence map›Paper›PMID 26437242›Full record

ArticleNature immunology2015

Control of peripheral tolerance by regulatory T cell-intrinsic Notch signaling.

Louis-Marie Charbonnier, Sen Wang, Peter Georgiev, Esen Sefik, Talal A Chatila

Open access · greenAbstract read
In one paragraph

Article in Nature immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
6.1field-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

85 citing papers in PubMed, 128 citations in OpenAlex.

  1. Article
  2. Review
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  4. Notch2 Directs aTreg Cell Fate Toward Immunoregulation or Inflammatory Pyroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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  17. Regulatory T cells in dominant immunologic tolerance.The Journal of allergy and clinical immunology · 2024
    Review
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  19. Review
  20. Review

25 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Louis-Marie CharbonnierDivision of Immunology, Boston Children's Hospital, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA.
Sen WangDivision of Immunology, Boston Children's Hospital, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA.
Peter GeorgievDivision of Immunology, Boston Children's Hospital, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA.
Esen SefikDivision of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts, USA.
Talal A ChatilaDivision of Immunology, Boston Children's Hospital, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA.
Boston Children's Hospital · USHarvard University · US

Funding

Molecular Basis of Hyper lgE ImmunodeficiencyR01AI065617 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Talal Amine Chatila · 2006 to 2026
$10.9M
Mechanisms of Disease Pathogenesis in Regulatory T cell DeficiencyR01AI085090 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHATILA, TALAL AMINE, WILLIAMS, CALVIN B · 2010 to 2020
$3.9M
Control of regulatory T cell homeostasis and function by Notch signalingR56AI115699 · NIAID · BOSTON CHILDREN'S HOSPITAL · PI CHATILA, TALAL AMINE · 2015 to 2015
$442k
NIAID NIH HHS 1R56AI115699-01NIAID NIH HHS 2R01AI065617NIAID NIH HHS 2R01AI085090NIAID NIH HHS R01 AI065617NIAID NIH HHS R01 AI085090NIAID NIH HHS R56 AI115699
6 · The paper itself

Abstract

Receptors of the Notch family direct the differentiation of helper T cell subsets, but their influence on regulatory T cell (T(reg) cell) responses is obscure. We found here that lineage-specific deletion of components of the Notch pathway enhanced T(reg) cell-mediated suppression of type 1 helper T cell (T(H)1 cell) responses and protected against their T(H)1 skewing and apoptosis. In contrast, expression in T(reg) cells of a gain-of-function transgene encoding the Notch1 intracellular domain resulted in lymphoproliferation, exacerbated T(H)1 responses and autoimmunity. Cell-intrinsic canonical Notch signaling impaired T(reg) cell fitness and promoted the acquisition by T(reg) cells of a T(H)1 cell-like phenotype, whereas non-canonical Notch signaling dependent on the adaptor Rictor activated the kinase AKT-transcription factor Foxo1 axis and impaired the epigenetic stability of Foxp3. Our findings establish a critical role for Notch signaling in controlling peripheral T(reg) cell function.

Indexed as

Peripheral ToleranceAnimalsCarrier ProteinsEpigenesis, GeneticFemaleForkhead Transcription FactorsGraft vs Host DiseaseMaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMice, TransgenicMutationRapamycin-Insensitive Companion of mTOR ProteinReceptor, Notch1Carrier ProteinsForkhead Transcription FactorsFoxp3 protein, mouseNotch1 protein, mouseRapamycin-Insensitive Companion of mTOR ProteinReceptor, Notch1Recombinant Fusion Proteinsrictor protein, mouse

Identifiers

PMID26437242
PMCPMC4618075
OpenAlexW1859056059

What OpenQuestion holds

Textmetadata
LicenceTDM
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.