Il13ra1, interleukin 13 receptor subunit alpha-1, is a key component of the interleukin-13 (IL-13) receptor complex. IL-13 is a cytokine that regulates many aspects of allergic inflammation, and Il13ra1 is crucial for IL-13 to initiate intracellular signaling and gene expression [1]. The IL-13/Il13ra1 pathway is involved in various biological processes, such as lymphocyte, myeloid cell, and non-hematopoietic cell responses [1].

In eosinophilic esophagitis (EoE), a chronic allergic disease, Il13ra1 plays a definitive role. Induction of experimental EoE in Il13ra1-/-mice blocked antigen-induced esophageal epithelial and lamina propria thickening, basal cell proliferation, eosinophilia, and tissue remodeling. Targeted deletion of Il13ra1 in esophageal epithelial cells also protected mice from experimental EoE. This shows that IL-13 signaling via Il13ra1 is involved in the pathogenesis of EoE [3]. In bullous pemphigoid (BP), the IL13-Il13ra1 ligand-receptor pair is identified as the most significant mediator of immune-stromal crosstalk. Fibroblasts and dendritic cells expressing Il13ra1 respond to IL-13-secreting Th2 cells, amplifying Th2-cell-mediated cascade responses [2].

In conclusion, Il13ra1 is essential for IL-13-mediated signaling and is involved in multiple disease processes. The use of Il13ra1 knockout mouse models has significantly contributed to understanding its role in diseases like EoE and BP, providing insights into potential therapeutic targets for these diseases.