Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-9475
Authors: Kao, Yu-San
Mamareli, Panagiota
Dhillon-LaBrooy, Ayesha
Stüve, Philipp
Godoy, Gloria Janet
Velasquez, Lis Noelia
Raker, Verena Katharina
Weidenthaler-Barth, Beate
Boukhallouk, Fatima
Rampoldi, Francesca
Berod, Luciana
Sparwasser, Tim
Title: Targeting ACC1 in T cells ameliorates psoriatic skin inflammation
Online publication date: 29-Aug-2023
Year of first publication: 2023
Language: english
Abstract: Psoriasis is a chronic inflammatory skin disease driven by the IL-23/IL-17 axis. It results from excessive activation of effector T cells, including T helper (Th) and cytotoxic T (Tc) cells, and is associated with dysfunctional regulatory T cells (Tregs). Acetyl-CoA carboxylase 1 (ACC1), a rate-limiting enzyme of fatty acid synthesis (FAS), directs cell fate decisions between Th17 and Tregs and thus could be a promising therapeutic target for psoriasis treatment. Here, we demonstrate that targeting ACC1 in T cells by genetic ablation ameliorates skin inflammation in an experimental model of psoriasis by limiting Th17, Tc17, Th1, and Tc1 cells in skin lesions and increasing the frequency of effector Tregs in skin-draining lymph nodes (LNs).
DDC: 610 Medizin
610 Medical sciences
Institution: Johannes Gutenberg-Universität Mainz
Department: FB 04 Medizin
Place: Mainz
ROR: https://ror.org/023b0x485
DOI: http://doi.org/10.25358/openscience-9475
Version: Published version
Publication type: Zeitschriftenaufsatz
License: CC BY
Information on rights of use: https://creativecommons.org/licenses/by/4.0/
Journal: Journal of molecular medicine
Version of Record (VoR)
Publisher: Springer
Publisher place: Berlin u.a.
Issue date: 2023
ISSN: 1432-1440
Publisher DOI: 10.1007/s00109-023-02349-w
Appears in collections:DFG-491381577-H

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