ArticleClinical rheumatology2026
Reduction of monocyte activation and oxidative stress by phosphodiesterase 4 blockade in Behçet's syndrome.
Article in Clinical rheumatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectivesBehçet's syndrome (BS) is a systemic vasculitis characterized by multisystemic inflammatory manifestations driven by innate and adaptive immunity. Apremilast, an oral small-molecule selective inhibitor of phosphodiesterase 4 (PDE4), has shown effectiveness in treating oral ulcers of BS in both randomized clinical trials and real-world studies. This study aimed to explore the potential molecular mechanisms of apremilast in BS.
methodsBulk RNA sequencing of peripheral blood mononuclear cells (PBMCs) from 15 BS patients undergoing apremilast treatment was performed. We evaluated reactive oxygen species (ROS) production by flow cytometry, as well as pro-inflammatory cytokine secretion and the transcriptomic signatures of monocytes before and after apremilast.
resultsTranscriptomic analysis revealed that apremilast treatment was associated with the suppression of oxidative stress and inflammatory pathways in PBMCs, along with a decrease in the proportion of monocytes. Integrative analysis identified BACH1 as a potential transcriptional regulator downregulated following treatment. In vitro, apremilast reduced ROS levels and proinflammatory cytokine expression in monocytes, effects that were partially recapitulated by BACH1 silencing.
conclusionApremilast is associated with the reduction of monocyte-driven inflammatory and oxidative stress signatures in BS, potentially involving the downregulation of BACH1. Key Points • Apremilast reduces inflammatory and oxidative stress signatures in the PBMCs of BS patients, primarily by targeting monocyte-driven inflammation. • The anti-inflammatory effects of apremilast in monocytes are potentially mediated through the downregulation of the transcription factor BACH1.
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