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Integrated Transcriptome and Metabolomics Analyses Show MYC as a Potential Therapeutic Target for Behçet's Uveitis
He Li1,2, Lei Zhu1,2, Zhaohuai Li3
1Department of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, China.
Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|June 30, 2025
Summary
Behçet's uveitis involves heightened glycolysis, driven by the MYC molecule. Targeting MYC offers a promising therapeutic strategy for this severe eye disease by regulating T cell responses.
Area of Science:
- Immunology
- Metabolomics
- Ophthalmology
Background:
- Behçet's uveitis (BU) is a severe form of Behçet's disease causing recurrent eye inflammation.
- The specific metabolic changes underlying BU pathogenesis are not well understood.
Purpose of the Study:
- To investigate metabolic alterations in Behçet's uveitis using metabolomics and single-cell RNA sequencing.
- To identify key molecular regulators of metabolic changes and their role in T cell responses.
Main Methods:
- Untargeted metabolomics and single-cell RNA sequencing (scRNA-seq) were performed on patients with BU and healthy controls.
- scRNA-seq data from experimental autoimmune uveitis (EAU) mouse models were analyzed.
- MYC expression and its role in glycolysis and T cell signaling were investigated.
Main Results:
- BU patients exhibited an altered metabolic profile with upregulated glycolysis.
- MYC was identified as a central regulator of glycolysis and T cell responses, with higher expression in BU.
- Inhibition of MYC reduced glycolysis, ameliorated EAU in mice, and suppressed effector T cell responses.
Conclusions:
- MYC promotes glycolysis to fuel aberrant T cell responses in Behçet's uveitis.
- Targeting MYC presents a potential therapeutic avenue for treating Behçet's uveitis by modulating T cell activity.
