Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

Innate immunity

Alarmins rewire innate immunity in newborns

This study describes an important role for the endogenous alarmins S100A8 and S100A9 in protecting newborn infants from sepsis. Healthy newborns produce extremely high levels of S100 alarmins for the first five days of life; the authors found that these alarmins signal through TLR4 to preactivate MYD88-dependent (but not TRIF-dependent) genes in neonatal monocytes, leaving them refractory to subsequent activation of MYD88. This 'rewiring' of neonatal monocytes prevented hyperinflammatory responses to bacteria without compromising host immunity. In a mouse model of Staphylococcus aureus-induced sepsis, S100A9-deficient neonates produced increased levels of pro-inflammatory cytokines, leading to fatal sepsis. In humans, pre-term infants that experienced late-onset neonatal sepsis had lower cord blood levels of S100 alarmins.

References

  1. 1

    Ulas, T. et al. S100-alarmin-induced innate immune programming protects newborn infants from sepsis. Nat. Immunol. 18, 622–632 (2017)

    CAS  Article  Google Scholar 

Download references

Authors

Rights and permissions

Reprints and Permissions

About this article

Verify currency and authenticity via CrossMark

Cite this article

Bordon, Y. Alarmins rewire innate immunity in newborns. Nat Rev Immunol 17, 467 (2017). https://doi.org/10.1038/nri.2017.84

Download citation

Search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing