IL-33 Elicits LTCSynthesis in Allergic Inflammation via ST2-Mediated Activation of Eosinophils.

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 LTCsynthesis remains elusive. Here, employing a murine model of allergic inflammation, ST2 activation emerged as a key step to LTCsynthesis, primarily achieved by lipid bodies-enriched eosinophils. Concurring, exogenous IL-33 elicited LTCsynthesis 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.