Journal of immunology research · 2026
Systematic Analysis of Peripheral Immune Signatures and Diagnostic Model Construction in Patients With Uterine Fibroids.
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Li Pei-Xian, Yu Si-Fei, Han Yu-Bin, Zhu Xiao-Hong, Lin Kai-Rong
Аннотация
OBJECTIVE: 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.
METHODS: 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.
RESULTS: 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.
CONCLUSION: 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.
METHODS: 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.
RESULTS: 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.
CONCLUSION: 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.