Abstract
Asthma is a heterogeneous disease that affects individuals of diverse age groups globally and exhibits variable responses to different treatments. Type 2 inflammation contributes to the pathogenesis of asthma through the production of cytokines IL-4, IL-5, and IL-13, thereby inducing characteristic features of asthma such as elevated eosinophil levels and airway hyperresponsiveness. The findings of the current study indicate that over 50% of individuals suffering from asthma exhibit Type 2 inflammation, with a higher prevalence observed in severe asthma. Moreover, biologics specifically designed to target Type 2 inflammation not only demonstrate favorable outcomes in treating severe asthma but also offer promising prospects for managing this condition. Therefore, it is of paramount importance to comprehend the intricate mechanisms of Type 2 inflammation in asthma. This article is aimed at providing an overview of the involvement of structural cells, innate immune cells, and adaptive immune cells in relation to Type 2 inflammation in asthma.