Exploring the role of immune cell and inflammatory cytokines in the development of rosacea

Immune cells and inflammatory cytokines collectively contribute to the pathogenesis of rosacea. However, the causality between immune cells, inflammatory cytokines and rosacea remains unclear. This study employed Mendelian randomization analysis to investigate the causality among 731 immune cells, 91 inflammatory cytokines, and rosacea. The inverse variance weighted, Mendelian randomization Egger, simple mode, weighted median, and weighted mode analyses were implemented to investigate causality. Sensitivity analyses were conducted to evaluate reliability of findings. Our research results indicated that 3 immune cells can increase risk of rosacea, 4 immune cells can decrease risk of rosacea. Among them, transitional (TR) B cell %lymphocyte (odds ratio [OR] = 1.170, 95% confidence interval [CI] = 1.001-1.368), CD25 on IgD- CD24- B cell (OR = 1.151, 95% CI = 1.013-1.307), and HLA DR on CD14- CD16+ monocyte (OR = 1.136, 95% CI = 1.007-1.281) increased risk of rosacea. Central memory CD4- CD8- T cell absolute count (OR = 0.952, 95% CI = 0.889-1.019), CCR7 on naive CD4+ T cell (OR = 0.928, 95% CI = 0.866-0.995), CD14+ CD16- monocyte absolute count (OR = 0.915, 95% CI = 0.857-0.977), and CD62L- myeloid dendritic cell (mDC; OR = 0.928, 95% CI = 0.862-0.999) decreased risk of rosacea. Meanwhile, the findings revealed that C-X-C motif chemokine 11 (CXCL11) levels (OR = 1.265, 95% CI = 0.985-1.625) and T-cell surface glycoprotein CD6 isoform levels (OR = 1.372, 95% CI = 1.069-1.761) increased risk of rosacea, while monocyte chemoattractant protein-1 levels (OR = 0.772, 95% CI = 0.621-0.960) and programmed cell death 1 ligand 1 levels (OR = 0.739, 95% CI = 0.557-0.981) decreased risk of rosacea. This study establishes a theoretical framework for comprehensively investigating the relationships between immune cells, inflammatory cytokines, and rosacea. It also offers valuable references for identifying novel therapeutic targets for rosacea.