ArticleJournal of molecular medicine (Berlin, Germany)2023
Targeting ACC1 in T cells ameliorates psoriatic skin inflammation.
Article in Journal of molecular medicine (Berlin, Germany), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Beyond Foxp3 and TSDR: a dual epigenetic lock framework for treg stability and plasticity.Frontiers in immunology · 2026Review
- Fatty acid metabolism-an emerging regulatory node in T-cell immunometabolism.Clinical & translational immunology · 2026Review
- Metabolic reprogramming of interleukin-17-producing γδ T cells promotes ACC1-mediated de novo lipogenesis under psoriatic conditions.Nature metabolism · 2025Article
- Mitochondrial fatty acid synthesis and MECR regulate CD4+ T cell function and oxidative metabolism.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- ACC1 is a dual metabolic-epigenetic regulator of Treg stability and immune tolerance.Molecular metabolism · 2025Article
- The immune mechanism of the mTOR/ACC1/CPT1A fatty acid oxidation signaling pathway in Hashimoto's thyroiditis.Journal of endocrinological investigation · 2025Article
- Metabolic regulation of Th9 cell differentiation: insights for IL-9-driven diseases.Frontiers in immunology · 2025Review
- Immunocyte lipid metabolic reprogramming: a novel pathway for targeted intervention in autoimmune diseases.Frontiers in immunology · 2025Review
- Overcoming immunotherapy resistance in glioblastoma: challenges and emerging strategies.Frontiers in pharmacology · 2025Review
- An axon-T cell feedback loop enhances inflammation and axon degeneration.Cell reports · 2024Article
- Regulation of human Th9 cell differentiation by lipid modulators targeting PPAR-γ and acetyl-CoA-carboxylase 1.Frontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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). KEY MESSAGES : ACC1 deficiency in T cells ameliorates psoriatic skin inflammation in mice. ACC1 deficiency in T cells reduces IL-17A-producing Th17/Tc17/dysfunctional Treg populations in psoriatic lesions. ACC1 deficiency in T cells restrains IFN-γ-producing Th1/Tc1 populations in psoriatic skin lesions and skin-draining LNs. ACC1 deficiency promotes activated CD44
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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.