Adalimumab Reprograms M1 Macrophages to Attenuate Th1/Th17 Responses in Behçet's Uveitis and Vogt-Koyanagi-Harada Syndrome - PubMed
3 hours ago
- #Uveitis
- #Adalimumab
- #Macrophage Polarization
- Adalimumab selectively suppresses M1 macrophage polarization in patients with Behçet's uveitis (BU) and Vogt-Koyanagi-Harada (VKH) syndrome.
- Reprogrammed M1 macrophages by adalimumab promote CD4+ T cell apoptosis and inhibit Th1/Th17 responses, without directly affecting T cells.
- Multi-omics analysis revealed disease-specific mechanisms: downregulation of metallothionein members (e.g., MT1H, MT1G) in BU and SLC39A8 in VKH.
- Adalimumab therapy reversed increased CD80+ macrophages and Th1/Th17 cells in an experimental autoimmune uveitis (EAU) model, leading to remission.
- Findings suggest adalimumab modulates macrophage polarization to attenuate T cell-mediated inflammation, offering insights for precision immunotherapy in uveitis.