Targeting ACC1 in T cells ameliorates psoriatic skin inflammation
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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
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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).
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Journal of molecular medicine, Version of Record (VoR), Springer, Berlin u.a., 2023, https://doi.org/10.1007/s00109-023-02349-w