膜性肾病
核糖核酸
免疫学
免疫
外围设备
生物
原电池
细胞
计算生物学
免疫系统
医学
遗传学
肾小球肾炎
基因
肾
内科学
作者
Fang Lu,Shiyi Chen,Honglei Guo,Qing Li,Lin Wu,Ying‐Xian Pan,Yangfan Wu,Hua Shu,Simeng Liu,Bo Zhang,Huijuan Mao,Changying Xing,Hongwei Liang,Suyan Duan,Yanggang Yuan
标识
DOI:10.3389/fimmu.2025.1622395
摘要
Background Primary Membranous Nephropathy (PMN) is characterized by dysregulated immune responses, with B cells playing critical roles in disease pathogenesis. However, the immunopathogenic mechanisms underlying B cell involvement in PMN remain elusive. Methods We employed single-cell RNA sequencing on peripheral blood mononuclear cell samples (PBMC) obtained from 6 patients with PMN and 3 healthy controls (NC) to explore the transformation of B cells and their interaction with immune cells. Results Compared with NC, the most significant alterations were in plasma cells and regulatory B (Breg) cells in PMN patients. Within plasma cells, Subcluster 0 was increased in PMN patients and exhibited enhanced autoimmunity. Breg subset B10 cells were elevated in PMN patients and displayed increased immune regulatory capacity, marked by enhanced cytokine and interleukin-10 production. B cell activating factor (BAFF) and galectin-9, which were secreted by CD14 monocyte, as potential regulators of plasma and Breg cells activity. Additionally, serum galectin-9 levels increased in PMN patients and showed a correlation with proteinuria and renal function in PMN. Conclusions We reveal novel insights into the heterogeneity and functional diversity of B cells in patients with PMN. And revealed distinct roles for subgroup 0 plasma cells and B10 Breg cells in the pathogenesis of PMN. Furthermore, targeting B cells, such as galectin-9, presents promising opportunities for modulating the immune response in patients with PMN.
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