Search for a command to run...
Allergic rhinitis (AR) is a major public health problem with a growing global prevalence, currently affecting approximately 30% of the world population. There remains limited understanding of how local cytokine production patterns following nasal allergen challenge relate to clinical symptoms, particularly in the context of the late-phase allergic response. Interleukin-13 (IL-13) has emerged as a significant contributor to the development of allergic inflammation in recent years. It shares many functional features with interleukin-4 (IL-4) due to the presence of a common receptor subunit. Although findings in the literature remain conflicting, they consistently support the role of IL-13 as a primary cause of allergic inflammation. The IL13 gene is expressed at higher levels in the nasal mucosa of both humans and mouse models with allergic rhinitis; however, the exact role of IL-13 in AR pathogenesis remains unclear. The present study aimed to investigate IL-13 expression levels in patients with clinically confirmed allergic rhinitis and demonstrate that increased expression levels of IL-13 gene products (protein and mRNA) play a critical role in disease development and immune activation, potentially serving as a diagnostic and therapeutic biomarker. In recent years, IL-13 has emerged as a key mediator in the pathology of allergic inflammation. It shares numerous functional properties with IL-4, owing to their use of a common receptor subunit. While literature findings vary, they consistently support the role of IL-13 as a key driver of allergic inflammation.