ArticleInvestigative ophthalmology & visual science2024
Itaconate Ameliorates Experimental Autoimmune Uveitis by Modulating Teff/Treg Cell Imbalance Via the DNAJA1/CDC45 Axis.
Article in Investigative ophthalmology & visual science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Itaconate and its derivatives in human health and diseases.Signal transduction and targeted therapy · 2026Review
- Itaconate and its derivatives ameliorate autoimmunity by suppressing Th17 cells via regulating mitophagy.Cell communication and signaling : CCS · 2026Article
- Regulatory T cells in autoimmune diseases: biological mechanisms, clinical translation, and translational challenges.Frontiers in immunology · 2026Review
- Regulatory T cell dysfunction and exhaustion in uveitis: immunometabolic mechanisms, microenvironmental drivers, and emerging therapeutic strategies.Frontiers in immunology · 2026Review
- Metabolic checkpoints in the regulation of Th17 cells: implications for uveitis pathogenesis and therapy.Frontiers in immunology · 2026Review
- Ferroptosis and the eye: bridging the gap between cell death and vision preservation.Frontiers in immunology · 2026Review
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: The aim of this study was to elucidate the effect of itaconate (ITA) on experimental autoimmune uveitis (EAU), to explore its potential mechanism, and to identify potential therapeutic targets. Methods: We established an animal model of EAU by constructing an immune map of mice treated with ITA and exploring the therapeutic mechanism of ITA by single-cell RNA sequencing and flow cytometry. Results: ITA mitigated ocular inflammation associated with EAU and reversed the pathogenic differentiation linked to Th17 induction by EAU, along with the reactive oxygen species (ROS) and oxidative stress pathways. Subsequent to ITA intervention, the downregulated differentially expressed genes in the T-cell subset primarily centered around the heat shock protein (HSP) family. Activation of HSPs reversed the anti-inflammatory effects of ITA in EAU mice. ITA decreased ROS levels and HSP expression in CD4+ T cells, with DnaJ heat shock protein family (HSP40) member A1 (DNAJA1) exhibiting the most notable alterations among the HSPs. ITA suppressed the expression of DNAJA1/cell division cycle protein 45 (CDC45), thereby disrupting the pathogenic division cycle of CD4+ T cells and reducing their proliferation. Inhibiting DNAJA1 also held promise for modulating the Th17/Treg imbalance. Notably, ITA curtailed the expansion of CD4+ T cells in uveitis patients. Conclusions: Our research delved into the potential therapeutic mechanisms underlying ITA therapy in EAU, offering fresh perspectives on its utility in the treatment of autoimmune conditions. DNAJA1 emerges as a promising candidate for targeted therapeutic interventions in uveitis.
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