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...
Gespeichert in:
Veröffentlicht in: | Immunology letters 2023-08 |
---|---|
Hauptverfasser: | , , , , , , , , , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | 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 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 |
DOI: | 10.1016/j.imlet.2023.08.001 |