Evidence map›Paper›PMID 26893133›Full record

ReviewEuropean journal of immunology2016

Metabolism of murine TH 17 cells: Impact on cell fate and function.

Ran Wang, Laura A Solt

Abstract readReview
In one paragraph

Review in European journal of immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Modeling the Th17 and Tregs Paradigm: Implications for Cancer Immunotherapy.Frontiers in cell and developmental biology · 2021
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
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

2 authors.

Ran WangDepartment of Molecular Therapeutics, The Scripps Research Institute, Jupiter, FL, USA.
Laura A SoltDepartment of Molecular Therapeutics, The Scripps Research Institute, Jupiter, FL, USA.

Funding

Regulation of TH17 Cell Development and Function by the REV-ERBsR01AI116885 · NIAID · SCRIPPS FLORIDA · PI SOLT, LAURA A · 2016 to 2020
$2.1M
Regulation of TH17 cell development and function by the REV-ERBsR56AI116885 · NIAID · SCRIPPS FLORIDA · PI SOLT, LAURA A · 2015 to 2015
$480k
NIAID NIH HHS R01 AI116885NIAID NIH HHS R01AI116885-01A1NIAID NIH HHS R56 AI116885NIAID NIH HHS R56AI116885
6 · The paper itself

Abstract

An effective adaptive immune response relies on the ability of lymphocytes to rapidly act upon a variety of insults. In T lymphocytes, this response includes cell growth, clonal expansion, differentiation, and cytokine production, all of which place a significant energy burden on the cell. Recent evidence shows that T-cell metabolic reprogramming is an essential component of the adaptive immune response and specific metabolic pathways dictate T-cell fate decisions, including the development of TH 17 versus T regulatory (Treg) cells. TH 17 cells have garnered significant attention due to their roles in the pathology of immune-mediated inflammatory diseases. Attempts to characterize TH 17 cells have demonstrated that they are highly dynamic, adjusting their function to environmental cues, which dictate their metabolic program. In this review, we highlight recent data demonstrating the impact of cellular metabolism on the TH 17/Treg balance and present factors that mediate TH 17-cell metabolism. Some examples of these include the differential impact of the mTOR signaling complexes on T-helper-cell differentiation, hypoxia inducible factor 1 alpha (HIF1α) promotion of glycolysis to favor TH 17-cell development, and ACC1-dependent de novo fatty acid synthesis favoring TH 17-cell development over Treg cells. Finally, we discuss the potential therapeutic options and the implications of modulating TH 17-cell metabolism for the treatment of TH 17-mediated diseases.

Indexed as

AcetyltransferasesAnimalsCD4 Lymphocyte CountCell DifferentiationCell ProliferationFatty AcidsGlycolysisHypoxia-Inducible Factor 1, alpha SubunitLymphocyte ActivationMiceSignal TransductionTh17 CellsT-Lymphocytes, RegulatoryTOR Serine-Threonine KinasesAcetyltransferasesaminoglycoside N1-acetyltransferaseFatty AcidsHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitmTOR protein, mouseTOR Serine-Threonine KinasesFatty acid ⋅ HIF1α ⋅ Glycolysis ⋅ mTOR ⋅ RORγt ⋅ TH17/Treg balance

Identifiers

PMID26893133
PMCPMC4901877

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.