ArticleClinical, cosmetic and investigational dermatology2025
Immune Cells Phenotypes and Causal Relationship with Acne Vulgaris: Insights from Mendelian Randomization.
Article in Clinical, cosmetic and investigational dermatology, 2025. 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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3 authors.
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Abstract
Object: We adopted a 2-sample bidirectional Mendelian randomization study to figure out whether circulating immune cells profiles causally impact acne vulgaris liability. Methods: Applying large-scale genome-wide association studies (GWAS) pooled data. We obtained the summary-level data for acne vulgaris (N=212,438) from the FinnGen Biobank. Using publicly available genetic data, we investigated the causal link between 731 immune cell profiles and DN risk. Included were four different types of immune systems: morphological parameters (MP), absolute cell (AC), relative cell (RC), and median fluorescence intensities (MFI). The results' robustness, heterogeneity, and horizontal pleiotropy were confirmed through extensive sensitivity analysis. Results: Our study identified causal associations between eight immune cells as potential mediators and acne vulgaris. Surprisingly, CD28 on CD39+ CD4+ T cell, CD39+ secreting CD4+ regulatory T cell and secreting CD4+ regulatory T cell were identified as the protective immunophenotype (OR=0.902, 0.944, 0.967, 95% CI 0.847-0.961, 0.906-0.983, 0.944-0.991). Moreover, CD24+ CD27+AC, CD24 on IgD+ CD38br mediated 5.723% and 6.844% of the decreased risk for acne vulgaris. Furthermore, FSC-A monocytes were found to mediate the increased risk of acne vulgaris, contributing 7.384% to this mediation. CD20-CD38-AC cells were identified to be associated with the 17.04% increased risk of acne vulgaris.
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