Mechanistic link uncovered between EBV infection and SLE

Epstein–Barr virus (EBV) has long been associated with systemic lupus erythematosus (SLE) but the mechanisms linking infection to autoimmunity have remained unclear. A new study reveals that EBV infection reprogrammes autoreactive B cells into pathogenic antigen-presenting cells that amplify systemic autoimmunity.

The EBV-infected B cells were predominantly CD27⁺CD21^low memory cells and showed upregulated expression of genes involved in antigen processing and presentation, B cell activation, interferon responses and T cell activation. The EBV-infected CD27⁺CD21^low memory B cells were also primed to differentiate into plasmablasts, linking viral infection to the expansion of antibody-secreting cells.