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Elevated circulating CD19 + CD24 hi CD38 hi B cells display pro-inflammatory phenotype in idiopathic membranous nephropathy

CD19 CD24 CD38 regulatory B cells exert immunosuppressive functions by producing IL-10, but their role in idiopathic membranous nephropathy (IMN) remains elusive. Here, we investigated the frequency and functional changes of circulating CD19 CD24 CD38 B cells and evaluated the correlation of CD19 CD...

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Bibliographic Details
Published in:Immunology letters 2023-08, Vol.261, p.58
Main Authors: Deng, Bishun, Deng, Li, Liu, Miao, Zhao, Ziling, Huang, Huijie, Tu, Xiaoxin, Liang, Enyu, Tian, Ruimin, Wang, Xiaowan, Wang, Rongrong, Lin, Haibiao, Yu, Yongyi, Peng, Anping, Xu, Peng, Bao, Kun, He, Min
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Language:English
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Summary:CD19 CD24 CD38 regulatory B cells exert immunosuppressive functions by producing IL-10, but their role in idiopathic membranous nephropathy (IMN) remains elusive. Here, we investigated the frequency and functional changes of circulating CD19 CD24 CD38 B cells and evaluated the correlation of CD19 CD24 CD38 B cells with clinical features and T helper cell subsets in IMN patients. Compared with healthy controls (HCs), IMN patients showed an increased frequency of CD19 CD24 CD38 B cells, but a significant reduction in the percentage of CD19 CD24 CD38 B cells was observed 4 weeks after cyclophosphamide treatment. The frequency of CD19 CD24 CD38 B cells was positively correlated with the levels of 24h urinary protein, but negatively correlated with serum total protein and serum albumin, respectively. CD19 CD24 CD38 B cells in IMN patients displayed a skewed pro-inflammatory cytokine profile with a higher level of IL-6 and IL-12, but a lower concentration of IL-10 than their healthy counterparts. Accompanied by upregulation of Th2 and Th17 cells in IMN patients, the percentage of CD19 CD24 CD38 B cell subset was positively associated with Th17 cell frequency. In conclusion, CD19 CD24 CD38 B cells were expanded but functionally impaired in IMN patients. Their altered pro-inflammatory cytokine profile may contribute to the pathogenesis of IMN.
ISSN:1879-0542