Evidence map›Paper›PMID 40360755›Full record

ArticleNature metabolism2025

Metabolic reprogramming of interleukin-17-producing γδ T cells promotes ACC1-mediated de novo lipogenesis under psoriatic conditions.

Yu-San Kao, Mario Lauterbach, Aleksandra Lopez Krol, Ute Distler, Gloria Janet Godoy, Matthias Klein, Rafael Jose Argüello, Fatima Boukhallouk, Sara Vallejo Fuente, Kathrin Luise Braband and 10 more

Abstract read
In one paragraph

Article in Nature metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

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  5. Metabolic control of innate-like T cells.Nature reviews. Immunology · 2026
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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

20 authors.

Yu-San KaoInstitute of Medical Microbiology and Hygiene, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. yusankao@uni-mainz.de.ORCID http://orcid.org/0000-0003-2571-853X
Mario LauterbachDepartment of Bioinformatics and Biochemistry, Braunschweig Integrated Centre of Systems Biology, Technical University of Braunschweig, Braunschweig, Germany.
Aleksandra Lopez KrolInstitute of Medical Microbiology and Hygiene, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.ORCID http://orcid.org/0009-0002-3151-9748
Ute DistlerResearch Center for Immunotherapy (FZI), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Gloria Janet GodoyInstitute of Medical Microbiology and Hygiene, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Matthias KleinResearch Center for Immunotherapy (FZI), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Rafael Jose ArgüelloAix Marseille University, CNRS, INSERM, CIML, Centre d'Immunologie de Marseille-Luminy, Marseille, France.ORCID http://orcid.org/0000-0001-9785-3883
Fatima BoukhalloukInstitute of Medical Microbiology and Hygiene, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Sara Vallejo FuenteInstitute of Medical Microbiology and Hygiene, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Kathrin Luise BrabandInstitute of Medical Microbiology and Hygiene, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.ORCID http://orcid.org/0000-0002-7436-1621
Assel NurbekovaInstitute for Immunology, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.ORCID http://orcid.org/0009-0000-2106-9179
Monica RomeroInstitute of Medical Microbiology and Hygiene, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Panagiota MamareliInstitute of Medical Microbiology and Hygiene, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Luana SilvaInstitute of Medical Microbiology and Hygiene, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.ORCID http://orcid.org/0000-0001-7297-9586
Luis Eduardo Alves DamascenoInstitute of Medical Microbiology and Hygiene, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.ORCID http://orcid.org/0000-0003-2833-9244
Francesca RampoldiInstitute of Medical Microbiology and Hygiene, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Luciana BerodResearch Center for Immunotherapy (FZI), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Lydia LynchMolecular Biology, Princeton University, Princeton, NJ, USA.ORCID http://orcid.org/0000-0002-4273-4681
Karsten HillerDepartment of Bioinformatics and Biochemistry, Braunschweig Integrated Centre of Systems Biology, Technical University of Braunschweig, Braunschweig, Germany.ORCID http://orcid.org/0000-0001-9322-5820
Tim SparwasserInstitute of Medical Microbiology and Hygiene, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. sparwasser@uni-mainz.de.ORCID http://orcid.org/0000-0001-5645-902X

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) 246807620Deutsche Forschungsgemeinschaft (German Research Foundation) 318346496Deutsche Forschungsgemeinschaft (German Research Foundation) 490846870Deutsche Forschungsgemeinschaft (German Research Foundation) LA 5301/1-1
6 · The paper itself

Abstract

Metabolic reprogramming determines γδ T cell fate during thymic development; however, the metabolic requirements of interleukin (IL)-17A-producing γδ T cells (γδT17 cells) under psoriatic conditions are unclear. Combining high-throughput techniques, including RNA sequencing, SCENITH, proteomics and stable isotope tracing, we demonstrated that psoriatic inflammation caused γδT17 cells to switch toward aerobic glycolysis. Under psoriatic conditions, γδT17 cells upregulated ATP-citrate synthase to convert citrate to acetyl-CoA, linking carbohydrate metabolism and fatty acid synthesis (FAS). Accordingly, we used a pharmacological inhibitor, Soraphen A, which blocks acetyl-CoA carboxylase (ACC), to impair FAS in γδT17 cells, reducing their intracellular lipid stores and ability to produce IL-17A under psoriatic conditions in vitro. We pinpointed the pathogenic role of ACC1 in γδT17 cells in vivo by genetic ablation, ameliorating inflammation in a psoriatic mouse model. Furthermore, ACC inhibition limited human IL-17A-producing γδT17 cells. Targeting ACC1 to attenuate pathogenic γδT17 cell function has important implications for psoriasis management.

Indexed as

Acetyl-CoA CarboxylaseInterleukin-17LipogenesisPsoriasisReceptors, Antigen, T-Cell, gamma-deltaAnimalsDisease Models, AnimalHumansMetabolic ReprogrammingMiceMice, Inbred C57BLTh17 CellsACC1 protein, mouseAcetyl-CoA CarboxylaseInterleukin-17Receptors, Antigen, T-Cell, gamma-delta

Identifiers

PMID40360755
PMCPMC12116387

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Registered trials

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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.