1. Academic Validation
  2. Abnormal glucose and lipid metabolism promotes disrupted differentiation of T and B cell subsets in Behçet's disease

Abnormal glucose and lipid metabolism promotes disrupted differentiation of T and B cell subsets in Behçet's disease

  • Immunother Adv. 2025 Mar 24;5(1):ltaf010. doi: 10.1093/immadv/ltaf010.
Minghao Li 1 2 3 4 Ping Li 5 6 Xin Wang 5 Lijie Wang 1 2 3 4 Guanmin Gao 7 Guosheng Jiang 8 Tingting Liu 9 Wei Lin 1 2 3 4
Affiliations

Affiliations

  • 1 Department of Rheumatology and Autoimmunology, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan, China.
  • 2 School of Clinical and Basic Medicine, Shandong First Medical University &Shandong Academy of Medical Sciences, Jinan, China.
  • 3 Shandong Key Laboratory of Rheumatic Disease and Translational Medicine, Shandong Medicine and Health Key Laboratory of Rheumatism, The First Affiliated Hospital of Shandong First Medical University, Jinan, China.
  • 4 Department of Critical-care Medicine, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
  • 5 Department of Clinical Laboratory, Qilu Hospital of Shandong University, Jinan, China.
  • 6 Shandong Engineering Research Center of Biomarker and artificial Intelligence Application, Jinan, China.
  • 7 Department of Rheumatology and Immunology, The First Affiliated Hospital of Zhengzhou University, #1 Jianshe East Road, Zhengzhou, China.
  • 8 Zibo First People's Hospital, Shandong, China.
  • 9 Shandong Eye Hospital, State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Shandong Eye Institute, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, China.
Abstract

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.

Keywords

B cells; Behçet’s disease; Th1; glucose metabolism; immune dysregulation; triglyceride metabolism.

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