BATF controls IFN I production via DC-SCRIPT in plasmacytoid dendritic cells

BATF suppresses type I interferon production in TLR9-activated plasmacytoid dendritic cells, with BATF deficiency increasing IFN-I and BATF overexpression inhibiting it.

• Why it matters: Excess IFN-I can contribute to pDC-driven autoimmunity, but BATF’s specific role in pDC IFN-I regulation and its underlying mechanism were unclear.
• What they did: The study used BATF-deficient and BATF-overexpressing systems in TLR9-activated pDCs, then combined integrated transcriptomics with ChIP-seq to show DC-SCRIPT is a direct BATF target that suppresses IFN-I promoter activity via IRF7.
• The result: In BATF-deficient mice, IFN-I serum levels rise early during LCMV infection, defining a BATF–DC-SCRIPT negative feedback axis that may shape antiviral and pDC-mediated human disease risk.

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