Immunotherapy advances · 2025
Abnormal glucose and lipid metabolism promotes disrupted differentiation of T and B cell subsets in Behçet's disease.
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Li Minghao, Li Ping, Wang Xin, Wang Lijie, Gao Guanmin, Jiang Guosheng, Liu Tingting, Lin Wei
Аннотация
INTRODUCTION: Behçet's disease (BD) is a chronic, systemic inflammatory condition characterized by recurrent immune dysregulation.
MATERIALS & METHODS: This study conducted a comprehensive analysis of immune cell subsets, metabolic markers, and their interplay in BD patients. Using multiparametric flow cytometry, we identified elevated Th1 cells, senescent CD8+ T cells, and abnormal B cell activation as hallmarks of the chronic inflammatory state in BD.
RESULTS: Despite immunotherapy, innate immune activation persisted, with increased mature NK cells, γδT1 cells, and conventional dendritic cells (cDCs), alongside reduced plasmacytoid dendritic cells (pDCs). Elevated glucose (GLU) and triacylglycerol (TAG) levels in BD patients correlated with increased Th1 cells, functional CD8+ T cells, and B cell activation. In vitro experiments demonstrated that GLU and TAG promote Th1 differentiation, CD8+ T cell activation, and B cell antibody production, revealing their role as drivers of immune dysregulation.
CONCLUSION: These findings underscore the intricate relationship between metabolic dysregulation and immune dysfunction in BD, highlighting potential diagnostic and therapeutic targets. Our study provides critical insights into BD pathogenesis, offering a foundation for optimizing disease management and monitoring immune and metabolic markers for improved patient outcomes.
MATERIALS & METHODS: This study conducted a comprehensive analysis of immune cell subsets, metabolic markers, and their interplay in BD patients. Using multiparametric flow cytometry, we identified elevated Th1 cells, senescent CD8+ T cells, and abnormal B cell activation as hallmarks of the chronic inflammatory state in BD.
RESULTS: Despite immunotherapy, innate immune activation persisted, with increased mature NK cells, γδT1 cells, and conventional dendritic cells (cDCs), alongside reduced plasmacytoid dendritic cells (pDCs). Elevated glucose (GLU) and triacylglycerol (TAG) levels in BD patients correlated with increased Th1 cells, functional CD8+ T cells, and B cell activation. In vitro experiments demonstrated that GLU and TAG promote Th1 differentiation, CD8+ T cell activation, and B cell antibody production, revealing their role as drivers of immune dysregulation.
CONCLUSION: These findings underscore the intricate relationship between metabolic dysregulation and immune dysfunction in BD, highlighting potential diagnostic and therapeutic targets. Our study provides critical insights into BD pathogenesis, offering a foundation for optimizing disease management and monitoring immune and metabolic markers for improved patient outcomes.