Evidence map›Paper›PMID 28404635›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2017

A Novel miR-24-TCF1 Axis in Modulating Effector T Cell Responses.

Sunglim Cho, Cheng-Jang Wu, Duc T Nguyen, Ling-Li Lin, Mei-Chi Chen, Aly Azeem Khan, Bi-Huei Yang, Wenxian Fu, Li-Fan Lu

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

8 citing papers in PubMed, 21 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Sunglim ChoDivision of Biological Sciences, University of California, San Diego, La Jolla, CA 92093.
Cheng-Jang WuDivision of Biological Sciences, University of California, San Diego, La Jolla, CA 92093.ORCID 0000-0002-7640-5915
Duc T NguyenDivision of Biological Sciences, University of California, San Diego, La Jolla, CA 92093.
Ling-Li LinDivision of Biological Sciences, University of California, San Diego, La Jolla, CA 92093.
Mei-Chi ChenDivision of Biological Sciences, University of California, San Diego, La Jolla, CA 92093.ORCID 0000-0002-9984-3459
Aly Azeem KhanToyota Technological Institute at Chicago, Chicago, IL 60637.
Bi-Huei YangDepartment of Pediatrics, University of California, San Diego, La Jolla, CA 92093.ORCID 0000-0003-3363-4408
Wenxian FuDepartment of Pediatrics, University of California, San Diego, La Jolla, CA 92093.ORCID 0000-0003-0684-8929
Li-Fan LuDivision of Biological Sciences, University of California, San Diego, La Jolla, CA 92093; lifanlu@ucsd.edu.ORCID 0000-0002-9727-0036
University of California San Diego · USToyota Technological Institute at Chicago · US

Funding

Role of microRNAs in regulatory T cell-mediated immunological tolerance and T celR01AI108651 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LU, LI-FAN · 2014 to 2024
$4.0M
Function of microRNAs in controlling regulatory T cell biologyR00AI089935 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LU, LI-FAN · 2012 to 2013
$493k
The role of SOCS1 repression by miR-155 in regulating immune responsivenessR21AI103646 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LU, LI-FAN · 2013 to 2014
$426k
Role of miR-146a at the interface between T and B cell immunityR21AI123782 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LU, LI-FAN · 2016 to 2017
$420k
Function of microRNAs in controlling regulatory T cell biologyK99AI089935 · NIAID · SLOAN-KETTERING INST CAN RESEARCH · PI LU, LI-FAN · 2011 to 2011
$94k
NIAID NIH HHS K99 AI089935NIAID NIH HHS R00 AI089935NIAID NIH HHS R01 AI108651NIAID NIH HHS R21 AI103646NIAID NIH HHS R21 AI123782
6 · The paper itself

Abstract

miR-23∼27∼24 was recently implicated in restricting Th2 immunity, as well as the differentiation and function of other effector T cell lineages. Interestingly, miR-24, unlike other family members, actually promotes Th1 and Th17 responses. In this article, we show that miR-24 drives the production of IFN-γ and IL-17 in T cells at least in part through targeting TCF1, a transcription factor known for its role in limiting Th1 and Th17 immunity. Surprisingly, whereas TCF1 was previously shown to promote Th2 responses through inducing GATA3, enforced TCF1 expression in miR-24-overexpressing T cells led to further downregulation of IL-4 and GATA3 expression, suggesting miR-24-mediated inhibition of Th2 immunity cannot be attributed to TCF1 repression by miR-24. Together, our data demonstrate a novel miR-24-TCF1 pathway in controlling effector cytokine production by T cells and further suggest miR-24 could function as a key upstream molecule regulating TCF1-mediated immune responses.

Indexed as

AnimalsCell DifferentiationCytokinesDown-RegulationGATA3 Transcription FactorHepatocyte Nuclear Factor 1-alphaInterferon-gammaInterleukin-17Interleukin-4Lymphocyte ActivationMiceMicroRNAsSignal TransductionTh17 CellsTh1 CellsTh2 CellsCytokinesGata3 protein, mouseGATA3 Transcription FactorHepatocyte Nuclear Factor 1-alphaHnf1a protein, mouseInterferon-gammaInterleukin-17Interleukin-4MicroRNAsMirn24 microRNA, mouse

Identifiers

PMID28404635
PMCPMC5437976
OpenAlexW2613822469

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.