Immune Cells Phenotypes and Causal Relationship with Acne Vulgaris: Insights from Mendelian Randomization.

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.