Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Phosphoenolpyruvate regulates the Th17 transcriptional program and inhibits autoimmunity

28 Feb 2023

Abstract excerpt

Aerobic glycolysis, a metabolic pathway essential for effector T cell survival and proliferation, regulates differentiation of autoimmune T helper (Th) 17 cells, but the mechanism underlying this regulation is largely unknown. Here, we identify a glycolytic intermediate metabolite, phosphoenolpyruvate (PEP), as a negative regulator of Th17 differentiation. PEP supplementation or inhibition of downstream...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Asthma and respiratory diseases
Share to Cytokine Signaling Pathways and Interactions
Share to Psoriasis: Treatment and Pathogenesis

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 36857180
DOI: 10.1016/j.celrep.2023.112205

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Phosphoenolpyruvate regulates the Th17 transcriptional program and inhibits autoimmunityPMID 36857180Read ↗

Deregulation of TGF-β1 signaling induces glycolysis by chromatin remodeling in pathogenic TH17 cellsSemantic proximity Read ↗

Glycolytic flux sustains human Th1 identity and effector function via STAT1 glycosylationSemantic proximity Read ↗

The glycolytic reaction PGAM unexpectedly restrains Th17 pathogenicity and Th17-dependent autoimmunitySemantic proximity Read ↗

Niche-selective inhibition of pathogenic Th17 cells by targeting metabolic redundancySemantic proximity Read ↗

A Glycolysis-Fatty Acid Metabolic Axis Shapes Human Tfh Cell FunctionSemantic proximity Read ↗

NF-κB-inducing kinase maintains T cell metabolic fitness in antitumor immunity.Semantic proximity Read ↗

Metabolic Reprogramming of Pathogenic CD4 <sup>+</sup> T Helper Cells Attenuates Inflammatory Bowel Disease PathogenesisSemantic proximity Read ↗

The Metabolic Requirements of Th2 Cell DifferentiationSemantic proximity Read ↗

HIF1α-glycolysis engages activation-induced cell death to drive IFN-γ induction in hypoxic T cellsSemantic proximity Read ↗

O-GlcNAcylation and low glycolysis underpin Th2 polarization by dendritic cellsSemantic proximity Read ↗

Glucose Metabolism Mediates Feedback Control of Innate Immune Signaling in Human MacrophagesSemantic proximity Read ↗

Glycolytic reprogramming shapes the histone acetylation profile of activated CD4+ T cells in juvenile idiopathic arthritisSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.