Human effector B lymphocytes express ARID3a and secrete interferon alpha

- ARID3a inhibition reduces IFNa expression.
- ARID3a+ human B lymphocytes secrete IFNa.
- ARID3a is induced by TLR agonists in healthy B cells.
- ARID3a expressing B lymphocytes enhance IFNa production in pDCs.

Previously, we determined that enhanced disease activity in patients with systemic lupus erythematosus (SLE) was associated with dramatic increases in numbers of B lymphocytes expressing the transcription factor ARID3a. Our data now indicate ARID3a is important for interferon alpha (IFNa) expression and show a strong association between ARID3a expression and transcription of genes associated with lupus IFN signatures. Furthermore, both ARID3a and IFNa production were elicited in healthy control B cells upon stimulation with the TLR 9 agonist, CpG. Importantly, secretion of IFNa from ARID3a+ healthy B lymphocytes stimulated increased IFNa production in plasmacytoid dendritic cells. These data identify ARID3a+ B cells as a novel type of effector B cell, and link ARID3a expression in B lymphocytes to IFN-associated inflammatory responses in SLE.

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