Evidence map›Paper›PMID 28848043›Full record

ArticleJournal of leukocyte biology2017

Fatty acid synthase regulates the pathogenicity of Th17 cells.

Kathryne E Young, Stephanie Flaherty, Kaitlyn M Woodman, Neelam Sharma-Walia, Joseph M Reynolds

Open access · bronzeAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

47 citing papers in PubMed, 86 citations in OpenAlex.

  1. Review
  2. Naive CD4iScience · 2026
    Article
  3. FASN-mediated metabolic reprogramming drives CD4Arthritis research & therapy · 2026
    Article
  4. Review
  5. Review
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  10. Control of T-cell immunity by fatty acid metabolism.Annals of pediatric endocrinology & metabolism · 2024
    Article
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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

5 authors at 1 institution in 1 country.

Kathryne E YoungDepartment of Microbiology and Immunology, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, USA.
Stephanie FlahertyDepartment of Microbiology and Immunology, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, USA.
Kaitlyn M WoodmanDepartment of Microbiology and Immunology, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, USA.
Neelam Sharma-WaliaDepartment of Microbiology and Immunology, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, USA.
Joseph M ReynoldsDepartment of Microbiology and Immunology, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, USA joseph.reynolds@rosalindfranklin.edu.
Rosalind Franklin University of Medicine and Science · US

Funding

Critical roles of endogenous TLR signaling in driving Th17 effector responsesK22AI104941 · NIAID · ROSALIND FRANKLIN UNIV OF MEDICINE & SCI · PI REYNOLDS, JOSEPH MICHAEL · 2013 to 2014
$270k
NIAID NIH HHS K22 AI104941
6 · The paper itself

Abstract

T cell activation and effector function is characterized by changes in metabolism. Altered metabolism is common to almost all types of activated T cells, but fatty acid synthesis seems to especially drive the formation of Th17 cells. Indeed, research has demonstrated that inhibition of early fatty acid synthesis through targeting of acetyl-CoA carboxylase (ACC1) can inhibit Th17 cell formation and instead promote the generation of regulatory T cells. Fatty acid synthase (FASN) is downstream of ACC, and previous studies have shown that FASN activity influences both cancer and inflammation. However, it remains to be determined whether FASN is a viable target for inhibiting Th17 cell function. Here, we demonstrate that FASN is a critical metabolic control for the generation of inflammatory subsets of Th17 cells. Conversely, inhibiting FASN function promotes IFN-γ production by Th1 and Th1-like Th17 cells. In vivo, inhibition of FASN, specifically in Th17 cells, leads to reduction of experimental autoimmune encephalomyelitis disease. These studies demonstrate the necessity of FASN in the autoimmune inflammatory function of Th17 cells.

Indexed as

4-ButyrolactoneAnimalsCell DifferentiationEncephalomyelitis, Autoimmune, ExperimentalEnzyme InhibitorsFatty Acid Synthase, Type IGene Expression RegulationHumansInterferon-gammaInterleukin-17Interleukin-23Lymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutMyelin-Oligodendrocyte Glycoprotein4-Butyrolactone4-methylene-2-octyl-5-oxofuran-3-carboxylic acidEnzyme InhibitorsFatty Acid Synthase, Type IInterferon-gammaInterleukin-17Interleukin-23Myelin-Oligodendrocyte Glycoproteinmyelin oligodendrocyte glycoprotein (35-55)Peptide FragmentsTlr2 protein, mouseToll-Like Receptor 2C75EAEIFN-γIL-17T lymphocyte

Identifiers

PMID28848043
PMCPMC5636042
OpenAlexW2750552950

What OpenQuestion holds

Textmetadata
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.