Anti-Inflammatory Interleukin Levels Reflect Th1/Th2 Imbalance in Spondyloarthritis Patients with Concomitant Atopy Under Biological Therapy

<b>Background/Objectives</b>: Atopy and spondyloarthritis (SpA) are immune-mediated diseases driven by distinct T-helper (Th) cell pathways-Th2 for atopy and Th1/Th17 for SpA. The coexistence of these divergent immune responses is increasingly recognized, particularly in the context of biological therapies that target pro-inflammatory cytokines. This study aimed to investigate Th2 cytokine profiles (IL-4, IL-5, IL-13) in atopic SpA patients receiving biological therapy to better understand how such treatment may influence immune regulation in this complex clinical setting. <b>Methods</b>: We conducted a prospective observational cross-sectional study on 136 SpA patients stratified by biological therapy and atopy status. Serum IL-4, IL-5, and IL-13 levels were quantified using LUMINEX immunoassays. Patients were grouped into biologically treated (BT) and Bio-Naïve (BN) cohorts and further sub-categorized by atopic phenotype (allergic rhinitis, asthma, dermatitis). Statistical comparisons of cytokine levels were made using SPSS IBM version 26 to explore associations with clinical and demographic variables. <b>Results</b>: IL-13 levels were significantly elevated in BT-atopic patients, particularly those with allergic rhinitis and atopic dermatitis, suggesting biological therapy may modulate Th2 responses. IL-5 remained elevated in allergic asthma cases despite treatment, indicating persistent eosinophilic activity. No significant correlation was found between cytokine levels and disease duration or therapy length. <b>Conclusions</b>: Biological therapy in SpA may influence Th2 cytokine expression, notably IL-13, in atopic patients. These findings underscore the importance of immune profiling in guiding personalized treatment strategies and highlight the need for further investigation into the long-term immunomodulatory effects of biologics in patients with overlapping Th1/Th2-driven diseases.