ArticleInvestigative ophthalmology & visual science2026
Adalimumab Reprograms M1 Macrophages to Attenuate Th1/Th17 Responses in Behçet's Uveitis and Vogt-Koyanagi-Harada Syndrome.
Article in Investigative ophthalmology & visual science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: To investigate the effects and underlying mechanisms of adalimumab on monocyte-derived macrophage polarization and CD4+ T cell responses in patients with Behçet's uveitis (BU) or Vogt-Koyanagi-Harada (VKH) syndrome. Methods: Ex vivo analyses were performed on monocyte-derived macrophages and CD4+ T cells from patients with active BU (n = 43) and VKH (n = 35). In vivo experiments were performed using an experimental autoimmune uveitis (EAU) model. The effects of adalimumab on macrophage polarization and cytokine production were assessed using flow cytometry and enzyme-linked immunosorbent assay, respectively. The underlying adalimumab-induced immunomodulatory cascade was evaluated using coculture systems with healthy donor CD4⁺ T cells. Disease-specific mechanisms were investigated through integrated transcriptomic and proteomic profiling and validated by real-time quantitative polymerase chain reaction and western blot. Results: Proinflammatory M1 macrophage polarization was significantly enhanced in patients with BU and VKH. Adalimumab selectively suppressed M1 polarization and the production of tumor necrosis factor-alpha, IL-1β, IL-6, and IL-12. These adalimumab-reprogrammed M1 macrophages promoted CD4+ T cell apoptosis and inhibited Th1/Th17 responses. However, adalimumab did not directly affect T cells. Multi-omics analysis and validation experiments revealed disease-specific mechanisms, notably the significant downregulation of the expression of metallothionein members, including MT1H, MT1G, MT1A, MT1F, MT1E, MT1X, and MT2A, in BU and that of SLC39A8 in VKH. Furthermore, adalimumab therapy reversed the increased frequencies of CD80+ macrophages and Th1/Th17 cells in the spleen and in association with remission of uveitis in the EAU model. Conclusions: Adalimumab modulates macrophage polarization to attenuate T cell-mediated inflammation by targeting different proteins in BU and VKH, providing novel insights for precision immunotherapy in uveitis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.