Evidence map›Paper›PMID 37862171›Full record

ArticleCell reports2023

An essential role for miR-15/16 in Treg suppression and restriction of proliferation.

Kristina Johansson, John D Gagnon, Simon K Zhou, Marlys S Fassett, Andrew W Schroeder, Robin Kageyama, Rodriel A Bautista, Hewlett Pham, Prescott G Woodruff, K Mark Ansel

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

12 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
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  7. Article
  8. HuR ablation destabilizesFrontiers in immunology · 2025
    Article
  9. Article
  10. Review
  11. Non-coding RNAs and neuroinflammation: implications for neurological disorders.Experimental biology and medicine (Maywood, N.J.) · 2024
    Review
  12. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 2 countries.

Kristina JohanssonDepartment of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143, USA; Sandler Asthma Basic Research Center, University of California, San Francisco, San Francisco, CA 94143, USA; Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of California, San Francisco, San Francisco, CA 94143, USA; Department of Medical Biochemistry and Cell Biology, University of Gothenburg, 40530 Gothenburg, Sweden; Department of Internal Medicine and Clinical Nutrition, University of Gothenburg, 40530 Gothenburg, Sweden.
John D GagnonDepartment of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143, USA; Sandler Asthma Basic Research Center, University of California, San Francisco, San Francisco, CA 94143, USA.
Simon K ZhouDepartment of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143, USA; Sandler Asthma Basic Research Center, University of California, San Francisco, San Francisco, CA 94143, USA.
Marlys S FassettDepartment of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143, USA; Department of Dermatology, University of California, San Francisco, San Francisco, CA 94143, USA.
Andrew W SchroederDepartment of Medicine, Genomics CoLab, University of California, San Francisco, San Francisco, CA 94143, USA.
Robin KageyamaDepartment of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143, USA; Sandler Asthma Basic Research Center, University of California, San Francisco, San Francisco, CA 94143, USA.
Rodriel A BautistaSandler Asthma Basic Research Center, University of California, San Francisco, San Francisco, CA 94143, USA; Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of California, San Francisco, San Francisco, CA 94143, USA.
Hewlett PhamDepartment of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143, USA; Sandler Asthma Basic Research Center, University of California, San Francisco, San Francisco, CA 94143, USA.
Prescott G WoodruffSandler Asthma Basic Research Center, University of California, San Francisco, San Francisco, CA 94143, USA; Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of California, San Francisco, San Francisco, CA 94143, USA.
K Mark AnselDepartment of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143, USA; Sandler Asthma Basic Research Center, University of California, San Francisco, San Francisco, CA 94143, USA. Electronic address: mark.ansel@ucsf.edu.
University of California, San Francisco · US

Funding

Role of miRNAs in Th2-Driven inflammation in AsthmaP01HL107202 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LOCKSLEY, RICHARD M · 2012 to 2023
$23.3M
Research BaseP30DK063720 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI VAISSE, CHRISTIAN · 2003 to 2019
$21.8M
MOLECULAR AND CELLULAR IMMUNOLOGYT32AI007334 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CYSTER, JASON G · 1988 to 2023
$11.0M
Role of miRNAs in Th2-Driven inflammation in AsthmaR01HL109102 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Karl Mark Ansel · 2011 to 2026
$5.5M
Mentoring Research in Precision Medicine for Lung DiseaseK24HL137013 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PRESCOTT G WOODRUFF · 2017 to 2026
$1.2M
BD FACSAria Fusion Cell SorterS10OD021822 · OD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LEE, MICHAEL R. · 2016 to 2016
$573k
NHLBI NIH HHS K24 HL137013NHLBI NIH HHS P01 HL107202NHLBI NIH HHS R01 HL109102NIAID NIH HHS T32 AI007334NIDDK NIH HHS P30 DK063720NIH HHS S10 OD021822
6 · The paper itself

Abstract

The miR-15/16 family targets a large network of genes in T cells to restrict their cell cycle, memory formation, and survival. Upon T cell activation, miR-15/16 are downregulated, allowing rapid expansion of differentiated effector T cells to mediate a sustained response. Here, we used conditional deletion of miR-15/16 in regulatory T cells (Tregs) to identify immune functions of the miR-15/16 family in T cells. miR-15/16 are indispensable to maintain peripheral tolerance by securing efficient suppression by a limited number of Tregs. miR-15/16 deficiency alters expression of critical Treg proteins and results in accumulation of functionally impaired FOXP3

Indexed as

MicroRNAsT-Lymphocytes, RegulatoryAnimalsCell DivisionForkhead Transcription FactorsInflammationMicePhenotypeForkhead Transcription FactorsMicroRNAsallergyCP: Immunologyeffector TregimmunosuppressionmiR-15miR-16miRNAT cellTCF1TregT regulatory cell

Identifiers

PMID37862171
PMCPMC10664750
OpenAlexW4387784023

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.