Il13ra1-KO Mouse

Il13ra1, the interleukin 13 receptor subunit alpha-1, is a key component of the receptor complexes for cytokines IL-4 and IL-13. These cytokines regulate various aspects of allergic inflammation, such as lymphocyte, myeloid cell, and non-hematopoietic cell responses. IL-4 and IL-13 can induce alternative macrophage activation through the receptor complex containing Il13ra1 [1].

In a study on eosinophilic esophagitis (EoE), Il13ra1 -/- mice and in vivo IL-13 antibody-based neutralization experiments 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, demonstrating a definitive role for IL-13 signaling via Il13ra1 in EoE [3]. In bullous pemphigoid, the IL13-IL13RA1 ligand-receptor pair was identified as the most significant mediator of immune-stromal crosstalk [2].

In conclusion, Il13ra1 is crucial for cytokine-mediated immune responses, especially those related to type 2 inflammation. The use of Il13ra1 knockout mouse models has revealed its role in diseases like EoE and bullous pemphigoid, highlighting its potential as a therapeutic target in such type 2 inflammatory disease conditions.

References:

1. Junttila, Ilkka S. 2018. Tuning the Cytokine Responses: An Update on Interleukin (IL)-4 and IL-13 Receptor Complexes. In Frontiers in immunology, 9, 888. doi:10.3389/fimmu.2018.00888. https://pubmed.ncbi.nlm.nih.gov/29930549/

2. Liu, Tingting, Wang, Zhenzhen, Xue, Xiaotong, Liu, Hong, Zhang, Furen. 2024. Single-cell transcriptomics analysis of bullous pemphigoid unveils immune-stromal crosstalk in type 2 inflammatory disease. In Nature communications, 15, 5949. doi:10.1038/s41467-024-50283-3. https://pubmed.ncbi.nlm.nih.gov/39009587/

3. Avlas, Shmulik, Shani, Guy, Rhone, Natalie, Rothenberg, Marc E, Munitz, Ariel. 2022. Epithelial cell-expressed type II IL-4 receptor mediates eosinophilic esophagitis. In Allergy, 78, 464-476. doi:10.1111/all.15510. https://pubmed.ncbi.nlm.nih.gov/36070083/