Requirement for IL-13 Independently of IL-4 in Experimental Asthma

TLDR

Asthma pathogenesis involves T cell cytokines, with IL‑4 and its receptor shown to contribute in murine models. Neutralizing IL‑13 reduces airway hyperresponsiveness, eosinophil recruitment, and mucus overproduction, and both IL‑13 and IL‑4 can induce an asthma‑like phenotype via the IL‑4 receptor α chain, linking this pathway to asthma genetics.

Abstract

The pathogenesis of asthma reflects, in part, the activity of T cell cytokines. Murine models support participation of interleukin-4 (IL-4) and the IL-4 receptor in asthma. Selective neutralization of IL-13, a cytokine related to IL-4 that also binds to the α chain of the IL-4 receptor, ameliorated the asthma phenotype, including airway hyperresponsiveness, eosinophil recruitment, and mucus overproduction. Administration of either IL-13 or IL-4 conferred an asthma-like phenotype to nonimmunized T cell–deficient mice by an IL-4 receptor α chain–dependent pathway. This pathway may underlie the genetic associations of asthma with both the human 5q31 locus and the IL-4 receptor.