Identifies Tph2-CD11c+CD21- B cell interactions that drive immune dysregulation in IgG4-related disease, suggesting new therapeutic avenues.
This study identifies a novel Tph2-CD11c⁺CD21⁻ B cell axis driving extrafollicular immune dysregulation in IgG4-RD. Tph2 cells link humoral activation with cytotoxicity, and CD11c⁺CD21⁻ B cells serve as producers of IgG4 associated with disease severity. Targeting this axis may provide therapeutic strategies for refractory or relapsing IgG4-RD beyond glucocorticoids.
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Sakamoto et al. (2026) studied this question.
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