Evidence map›Paper›PMID 26831822›Full record

ArticleImmunobiology2016

Snai2 and Snai3 transcriptionally regulate cellular fitness and functionality of T cell lineages through distinct gene programs.

Peter D Pioli, Sarah K Whiteside, Janis J Weis, John H Weis

Open access · greenAbstract read
In one paragraph

Article in Immunobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.3field-weighted citation impact, top 38% 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

6 citing papers in PubMed, 12 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

4 authors at 1 institution in 1 country.

Peter D PioliDivision of Cell Biology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT 84132, United States. Electronic address: pdpioli@g.ucla.edu.
Sarah K WhitesideDivision of Cell Biology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT 84132, United States.
Janis J WeisDivision of Cell Biology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT 84132, United States.
John H WeisDivision of Cell Biology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT 84132, United States.
University of Utah · US

Funding

MOLECULAR GENETICS OF LYME ARTHRITIS SUSCEPTIBILITYR01AR043521 · NIAMS · UNIVERSITY OF UTAH · PI WEIS, JANIS J. · 1994 to 2024
$9.4M
RESEARCH TRAINING IN HEMATOLOGYT32DK007115 · NIDDK · UNIVERSITY OF UTAH · PI LEIBOLD, ELIZABETH ANN, PRCHAL, JOSEF T · 1986 to 2020
$8.4M
BORRELIA BURGDORFERI MITOGEN IN DEVELOPMENT OF ARTHRITISR01AI032223 · NIAID · UNIVERSITY OF UTAH · PI WEIS, JANIS J. · 1993 to 2023
$7.8M
Training Program in Microbial PathogenesisT32AI055434 · NIAID · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI MULVEY, MATTHEW A, PLANELLES, VICENTE · 2004 to 2025
$6.0M
Univ of Utah Cell Sorter for Flow Cytometry CoreS10RR026802 · NCRR · UNIVERSITY OF UTAH · PI GREEN, WAYNE FRANCIS · 2010 to 2010
$500k
Role of Zfp318 in the functional development of B cellsR21AI114462 · NIAID · UNIVERSITY OF UTAH · PI WEIS, JANIS J. · 2015 to 2016
$410k
Borrelia Burgdorferi Mitogen in Development of ArthritisR56AI032223 · NIAID · UNIVERSITY OF UTAH · PI WEIS, JANIS J. · 2013 to 2013
$350k
NCRR NIH HHS 1S10RR026802-01NCRR NIH HHS S10 RR026802NIAID NIH HHS AI032223NIAID NIH HHS AI114462NIAID NIH HHS R01 AI032223NIAID NIH HHS R21 AI114462NIAID NIH HHS R56 AI032223NIAID NIH HHS T32 AI055434NIAMS NIH HHS AR043521NIAMS NIH HHS R01 AR043521NIDDK NIH HHS T32 DK007115NIDDK NIH HHS T-32DK007115-40
6 · The paper itself

Abstract

T lymphocytes are essential contributors to the adaptive immune system and consist of multiple lineages that serve various effector and regulatory roles. As such, precise control of gene expression is essential to the proper development and function of these cells. Previously, we identified Snai2 and Snai3 as being essential regulators of immune tolerance partly due to the impaired function of CD4(+) regulatory T cells in Snai2/3 conditional double knockout mice. Here we extend those previous findings using a bone marrow transplantation model to provide an environmentally unbiased view of the molecular changes imparted onto various T lymphocyte populations once Snai2 and Snai3 are deleted. The data presented here demonstrate that Snai2 and Snai3 transcriptionally regulate the cellular fitness and functionality of not only CD4(+) regulatory T cells but effector CD8(α+) and CD4(+) conventional T cells as well. This is achieved through the modulation of gene sets unique to each cell type and includes transcriptional targets relevant to the survival and function of each T cell lineage. As such, Snai2 and Snai3 are essential regulators of T cell immunobiology.

Indexed as

Gene Expression RegulationAnimalsBiomarkersCell LineageCytokinesGene DeletionImmunologic MemoryImmunophenotypingLymphocyte ActivationMiceMice, KnockoutPhenotypeReceptors, Antigen, T-Cell, alpha-betaSnail Family Transcription FactorsT-Lymphocyte SubsetsTranscription, GeneticBiomarkersCytokinesReceptors, Antigen, T-Cell, alpha-betaSnai2 protein, mouseSnai3 protein, mouseSnail Family Transcription FactorsAutoimmunityGenetic deficiencySnail transcription factorsT cell receptorT lymphocyte

Identifiers

PMID26831822
PMCPMC4801692
OpenAlexW2278267398

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.