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STING Activation Triggers Cell-Death Pathway Behind Rare Childhood Vasculopathy, Nature Study Finds

Researchers traced the damage in SAVI to a specific programmed cell death cascade and showed in animals that shutting it down eases disease.

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Overview

  • Published on August 21 in Nature, the multicenter study from the University of Cologne and Ospedale Pediatrico Bambino Gesù was led by Gianmaria Liccardi.
  • Experiments show that activation of the immune sensor STING drives ZBP1-dependent necroptosis, defining a direct mechanistic basis for SAVI.
  • Analyses of samples from affected children found clear evidence of aberrant activation of programmed cell death.
  • In animal models, blocking necroptosis reduced symptoms, lowered disease severity, and significantly extended survival.
  • The results support developing necroptosis inhibitors as a potential treatment for SAVI and other STING-linked inflammatory conditions, with clinical translation still to come.