نوع مقاله : مقاله پژوهشی
عنوان مقاله English
نویسنده English
Abstract
Asthma is a chronic respiratory disease characterized by persistent inflammation and structural remodeling of the airways, imposing a substantial burden on both individual and public health. Over recent decades, the role of immune cells and their secreted cytokines has been increasingly recognized as a central axis in the pathogenesis and clinical heterogeneity of asthma. Type 2 helper T cells (Th2) and their associated cytokines, including interleukin-4 (IL-4), interleukin-5 (IL-5), and interleukin-13 (IL-13) form the foundation of allergic inflammation and symptom exacerbation. In parallel, T helper 17 cells (Th17) and interleukin-17 (IL-17) play a pivotal role in neutrophilic asthma, which is frequently resistant to conventional therapies. Moreover, impaired function of regulatory T cells (Tregs) and reduced production of anti-inflammatory cytokines such as interleukin-10 (IL-10) and transforming growth factor-beta (TGF-β) contribute to
persistent inflammation and tissue damage. Innate immune cells, including macrophages and type 2 innate lymphoid cells (ILC2s), further contribute by secreting early cytokines that initiate inflammatory responses. Recent therapeutic advances targeting key cytokines, particularly monoclonal antibodies against IL-5 and IL-13, have demonstrated efficacy in reducing inflammation and improving disease control. Nevertheless, the diverse and multidimensional role of immunity in asthma underscores the need for further research to develop personalized therapeutic strategies and reduce the global burden of this disease. The aim of the present study is to investigate and analyze the role of immune cells and their cytokines in the onset and pathogenesis of asthma, as well as to evaluate their impact on disease severity and patients’ quality of life.