Evidence map›Paper›PMID 22579475›Full record

ArticleImmunity2012

An N-terminal mutation of the Foxp3 transcription factor alleviates arthritis but exacerbates diabetes.

Jaime Darce, Dipayan Rudra, Li Li, Junko Nishio, Daniela Cipolletta, Alexander Y Rudensky, Diane Mathis, Christophe Benoist

Open access · bronzeAbstract read
In one paragraph

Article in Immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 1 pooled it
8.5field-weighted citation impact, top 2% 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

74 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Characterizing Foxp3Frontiers in immunology · 2024
    Article
  6. Article
  7. Genetic Tools for Analyzing Foxp3Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Ubiquitin-Dependent Regulation of Treg Function and Plasticity.Advances in experimental medicine and biology · 2021
    Article
  16. A Structure-Guided Delineation of FOXP3 Regulation Mechanism in IPEX.Advances in experimental medicine and biology · 2021
    Article
  17. Article
  18. Transcriptional regulation of Treg homeostasis and functional specification.Cellular and molecular life sciences : CMLS · 2020
    Review
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Jaime DarceDivision of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA.
Dipayan Rudra
Li Li
Junko Nishio
Daniela Cipolletta
Alexander Y Rudensky
Diane Mathis
Christophe Benoist
Harvard University · USMemorial Sloan Kettering Cancer Center · US

Funding

Post-transcriptional regulation of inflammatory arthritisP01AI065858 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI LEE, DAVID M · 2006 to 2010
$11.1M
Adipose-tissue Tregs: important players in immunological control of metabolismR01DK092541 · NIDDK · HARVARD MEDICAL SCHOOL · PI DIANE J MATHIS · 2011 to 2026
$6.4M
Naive T cell homeostasis: Treg selection and survivalR37AI051530 · NIAID · HARVARD MEDICAL SCHOOL · PI BENOIST, CHRISTOPHE O. · 2009 to 2018
$4.1M
Naive T cell survival: TCR and IL-7R signal interplayR01AI051530 · NIAID · JOSLIN DIABETES CENTER · PI BENOIST, CHRISTOPHE O. · 2002 to 2009
$2.4M
Howard Hughes Medical InstituteNCI NIH HHS T32CA007386NIAID NIH HHS AI051530NIAID NIH HHS AI065858NIAID NIH HHS P01 AI065858NIAID NIH HHS R01 AI051530NIAID NIH HHS R37 AI051530NIDDK NIH HHS DK092541NIDDK NIH HHS R01 DK092541
6 · The paper itself

Abstract

Maintenance of lymphoid homeostasis in a number of immunological and inflammatory contexts is served by a variety of regulatory T (Treg) cell subtypes and depends on interaction of the transcription factor FoxP3 with specific transcriptional cofactors. We report that a commonly used insertional mutant of FoxP3 (GFP-Foxp3) modified its molecular interactions, blocking HIF-1α but increasing IRF4 interactions. The transcriptional profile of these Treg cells was subtly altered, with an overrepresentation of IRF4-dependent transcripts. In keeping with IRF4-dependent function of Treg cells to preferentially suppress T cell help to B cells and Th2 and Th17 cell-type differentiation, GFP-FoxP3 mice showed a divergent susceptibility to autoimmune disease: protection against antibody-mediated arthritis in the K/BxN model, but greater susceptibility to diabetes on the NOD background. Thus, specific subfunctions of Treg cells and the immune diseases they regulate can be influenced by FoxP3's molecular interactions, which result in divergent immunoregulation.

Indexed as

MutationAnimalsArthritisAutoimmune DiseasesB-LymphocytesCell DifferentiationDiabetes Mellitus, Type 1Forkhead Transcription FactorsHomeostasisHypoxia-Inducible Factor 1, alpha SubunitInterferon Regulatory Factor-4Interferon Regulatory FactorsMiceMice, Inbred C57BLMice, Inbred NODProtein Interaction Domains and MotifsForkhead Transcription FactorsFoxp3 protein, mouseHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitInterferon Regulatory Factor-4Interferon Regulatory FactorsTranscription Factors

Identifiers

PMID22579475
PMCPMC3386606
OpenAlexW2151487189

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.