Proinflammatory phenotype of B10 and B10pro cells elicited by tumour necrosis factor (TNF)-α in rheumatoid arthritis
Authors' conclusion
TNF-α provoked the proinflammatory phenotype of B10 and B10pro cells by disturbing SHIP-1 in RA, contributing to the disease development.
Study context
- Population
- Healthy individuals and patients with rheumatoid arthritis (RA); TNF-α-/- and B cell-specific SHIP-1-/- mice
- Comparison
- Patients with RA vs healthy individuals; patients with RA before vs after anti-TNF therapy
- Outcome
- Frequencies and functions of B10 and B10pro cells; effects of TNF-α on their quantity, stability and pathogenic phenotype
Methodological detailsscRNA-seq database reanalysis, transcriptome sequencing, TNF-α-/- and B cell-specific SHIP-1-/- mouse disease models, before and after anti-TNF therapy
- scRNA-seq database reanalysis
- Transcriptome sequencing
- TNF-α-/- and B cell-specific SHIP-1-/- mouse disease models
- Before and after anti-TNF therapy
Main finding
As reported in the abstract
- TNF-α was a key determinant for B10 cells
- TNF-α elicited proinflammatory feature of B10 and B10pro cells: IL-10 downregulated, interferon-γ and IL-17A upregulated
- In RA, B10 and B10pro cells impaired with exacerbated proinflammatory phenotype
- Anti-TNF therapy potently restored their frequencies and immunosuppressive functions, consistent with increased B10 cells in TNF-α-/- mice
- TNF-α diminished B10 and B10pro cells by inhibiting their glycolysis and proliferation
- TNF-α regulated phosphatidylinositol phosphate signalling and dampened expression of SHIP-1
Original publication
Proinflammatory phenotype of B10 and B10pro cells elicited by TNF-α in rheumatoid arthritis. Ann Rheum Dis. Published 11 April 2024. doi:10.
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