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Evidence-Based Supplement Research
Evidence-Based Supplement Research

The alterations of blood immune subpopulations, cytokines, and metabolites in anti-acetylcholine receptor antibody-positive myasthenia gravis: a real-world, observational, high-throughput study.

  • 2026-05
  • Immunobiology 231(3)
    • Huanyu Meng
    • Xiaoyu Chen
    • Zhuoying Zhu
    • Guangqiang Sun
    • Lu He
    • Qinming Zhou
    • Liang Li
    • Xinying Yang
    • Xingkun Chu
    • Dabing Yang
    • Yuan Feng
    • Jing Zhang
    • Sheng Chen

Study Design

Type
Observational
Sample size
n = 37
Population
37 anti-AChR antibody positive MG patients and 37 healthy controls
Methods
blood immune cells were analyzed by mass cytometry, plasma proteins were determined by Cytokine Array, and metabolites were measured by targeted metabolomics
Comprehensive profiling of peripheral blood may reveal candidate markers and therapeutic targets for anti-AChR antibody positive myasthenia gravis (MG) patients. We enrolled 37 anti-AChR antibody positive MG patients and 37 healthy controls (HCs), and blood immune cells were analyzed by mass cytometry, plasma proteins were determined by Cytokine Array, and metabolites were measured by targeted metabolomics. Compared with HCs, anti-AChR antibody positive MG patients showed increased classical monocytes and Th2-like cells, and decreased Th1-like cells, regulatory T cells, CD4+T, and CD28+T cells. Cytokine profiling revealed reduced retinol-binding protein 4 (RBP4), epithelial neutrophil-activating peptide 78 (ENA-78), and stem cell factor receptor (SCF-R), but elevated angiogenin, RANTES (CCL5), and cystatin-A. Metabolomics indicated lower dehydroepiandrosterone sulfate (DHEAS), cystine, and arginine, with higher lactate, sarcosine, and ornithine. Notably, glucocorticoid pretreatment reduced myeloid dendritic cells, Th2-like cells, dendritic cells, classical monocytes, and total monocytes. Integrated multi-omics analysis identified immune-metabolic interactions associated with anti-AChR antibody positive MG pathogenesis. This study highlights potential candidate markers and provides insights for targeted therapy.

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