STAT3 acts as an inflammation-dependent switch in antiviral NK cells
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New work in Science Immunology shows that STAT3, usually treated as a straightforward cytokine effector, behaves as a context-dependent transcriptional switch in antiviral NK cells during MCMV infection. Which way it flips depends on the inflammatory milieu: when IL-15 dominates, STAT3 supports adaptive NK cell responses, but when type I interferon dominates, it impairs them. Recruited to distinct genomic loci under each cytokine, STAT3 drives alternative transcriptional programs by differentially regulating MYB and BLIMP-1, with its relocation governed by epigenetic mechanisms and STAT motif preference. The study reframes STAT3 as an integrator of inflammatory signals in lymphocyte adaptation rather than a fixed effector. How these competing cytokine programs are balanced in other infection and tumor settings is still open.
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- Sci ImmunolSTAT3 operates as an inflammation-dependent transcriptional switch in antiviral NK cells.
STAT3 acts as a cytokine-sensing transcriptional switch in antiviral NK cells during MCMV infection, promoting or impairing adaptive NK cell responses depending on whether IL-15 or type I interferon dominates the inflammatory milieu. Recruited to distinct genomic loci under each cytokine, STAT3 drives alternative transcriptional programs by differentially regulating MYB and BLIMP-1, with relocation governed by epigenetic mechanisms and STAT motif preference. The work reframes a canonical cytokine effector as a context-dependent integrator of inflammatory signals in lymphocyte adaptation.
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