BiologyMedicine

Vitória F. Rosário‐Garcia, Ericka Guimaraes-Ferreira, Yasmin Brito-Leite, Jamille F. Oliveira, Julia Santos-da-Silva, N. Amorim, Valdirene S. Muniz, Lukas Bolini, Miriam B F Werneck, Claudio A. Canetti, Bruno L. Diaz, C. Bandeira‐Melo

2026.2.28EUROPEAN JOURNAL OF IMMUNOLOGY

DOI: 10.1002/eji.70156

tlooto Summary

Conurring, exogenous IL‐33 elicited LTC4 synthesis from activated eosinophils, both in vivo and from human cells in vitro, relevant to eosinophil‐regulated environments, may bear therapeutic potential as a target in cysteinyl leukotrienes‐mediated conditions.

Abstract

Like pieces of a puzzle, IL‐33, eosinophils, and cysteinyl leukotrienes seem to come together and orchestrate allergic inflammation. While the IL‐33/ST2 receptor axis is known to activate some classical eosinophil functions, its ability to specifically trigger LTC4 synthesis remains elusive. Here, employing a murine model of allergic inflammation, ST2 activation emerged as a key step to LTC4 synthesis, primarily achieved by lipid bodies‐enriched eosinophils. Concurring, exogenous IL‐33 elicited LTC4 synthesis from activated eosinophils, both in vivo and from human cells in vitro. Thus, relevant to eosinophil‐regulated environments, such IL‐33/ST2‐driven cellular effect may bear therapeutic potential as a target in cysteinyl leukotrienes‐mediated conditions.

Citation format

ROSÁRIO‐GARCIA, Vitória F., et al. IL‐33 elicits LTC4 synthesis in allergic inflammation via st2‐mediated activation of eosinophils. EUROPEAN JOURNAL OF IMMUNOLOGY, 2026, 56(3): e70156.