Observational insights reveal the IL-33/ST2 axis influences vascular inflammation in Kawasaki disease, suggesting new treatment strategies.
Current evidence supports the IL-33/ST2 axis as a plausible, context-dependent modulatory pathway linking tissue injury, innate immune activation, and vascular inflammation in KD. Soluble ST2 shows particular promise as a biomarker reflecting disease activity and cardiac stress. Targeted modulation of IL-33/ST2 signaling, guided by disease phase and biomarker profiles, could represent a next-generation therapeutic approach to prevent CAAs in KD.
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Okada et al. (2026) studied this question.
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