Systematic Analysis of Peripheral Immune Signatures and Diagnostic Model Construction in Patients With Uterine Fibroids.
To systematically characterize the peripheral immune signature of uterine fibroids (UFs) and to develop a diagnostic model for differentiating UF patients from healthy individuals, thereby providing new insights into UF immunopathogenesis.
We performed multiparametric flow cytometry analysis on peripheral blood samples from 31 UF patients and 63 age-matched healthy controls (HCs). A total of 70 immune parameters were evaluated, encompassing T cells, B cells, natural killer (NK) cells, γδ T cells, and their functional subsets.
Comprehensive immunophenotyping revealed a distinct peripheral immune profile in UF patients. Key findings included a significant dysregulation within helper T (Th) cell compartments, characterized by elevated frequencies of functional Th and Th17 cells, alongside reduced proportions of senescent Th, T follicular helper 1 (Tfh1), and peripheral Th (Tph) cells. Concurrently, a significant expansion of the B cell compartment was observed, marked by increased total B cells, naïve B cells, immature regulatory B cells (Breg), and transformed B cells. In contrast, the frequencies and functional subsets of cytotoxic T (Tc) cells, γδ T cells, and NK cells showed no significant alterations after false discovery rate (FDR) correction. A random forest (RF) model incorporating key immune markers effectively discriminated UF patients from HCs, identifying several markers as central features with both diagnostic and mechanistic relevance.
This study presents the first systematic atlas of the peripheral immune landscape in UF, revealing a pattern of systemic immune dysregulation centered on Th and B cell pathways. These findings advance our understanding of the immunopathogenesis of UF and establish a foundation for future immune-based diagnostic and therapeutic strategies.
We performed multiparametric flow cytometry analysis on peripheral blood samples from 31 UF patients and 63 age-matched healthy controls (HCs). A total of 70 immune parameters were evaluated, encompassing T cells, B cells, natural killer (NK) cells, γδ T cells, and their functional subsets.
Comprehensive immunophenotyping revealed a distinct peripheral immune profile in UF patients. Key findings included a significant dysregulation within helper T (Th) cell compartments, characterized by elevated frequencies of functional Th and Th17 cells, alongside reduced proportions of senescent Th, T follicular helper 1 (Tfh1), and peripheral Th (Tph) cells. Concurrently, a significant expansion of the B cell compartment was observed, marked by increased total B cells, naïve B cells, immature regulatory B cells (Breg), and transformed B cells. In contrast, the frequencies and functional subsets of cytotoxic T (Tc) cells, γδ T cells, and NK cells showed no significant alterations after false discovery rate (FDR) correction. A random forest (RF) model incorporating key immune markers effectively discriminated UF patients from HCs, identifying several markers as central features with both diagnostic and mechanistic relevance.
This study presents the first systematic atlas of the peripheral immune landscape in UF, revealing a pattern of systemic immune dysregulation centered on Th and B cell pathways. These findings advance our understanding of the immunopathogenesis of UF and establish a foundation for future immune-based diagnostic and therapeutic strategies.