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.
Rosário-Garcia et al. (Sun,) studied this question.