Interleukin-13: Central Mediator of Allergic Asthma

TLDR

Allergic asthma incidence is rising worldwide, and its pathophysiology is linked to aberrant CD4⁺ T‑cell expansion producing IL‑4 and IL‑5, though the necessity of these cytokines remains unproven. IL‑13 is both necessary and sufficient for allergic asthma, driving disease features independently of IgE and eosinophils and operating through non‑classical mechanisms.

Abstract

The worldwide incidence, morbidity, and mortality of allergic asthma are increasing. The pathophysiological features of allergic asthma are thought to result from the aberrant expansion of CD4 + T cells producing the type 2 cytokines interleukin-4 (IL-4) and IL-5, although a necessary role for these cytokines in allergic asthma has not been demonstrable. The type 2 cytokine IL-13, which shares a receptor component and signaling pathways with IL-4, was found to be necessary and sufficient for the expression of allergic asthma. IL-13 induces the pathophysiological features of asthma in a manner that is independent of immunoglobulin E and eosinophils. Thus, IL-13 is critical to allergen-induced asthma but operates through mechanisms other than those that are classically implicated in allergic responses.