Ankylosing spondylitis is a chronic inflammatory disease primarily affecting the axial skeleton, characterized by enthesitis, progressive spinal stiffness, and systemic immune dysregulation. Emerging evidence implicates CD4 T cell subsets-particularly Th17 and regulatory T cells in the pathological immune responses that drive AS progression. Conventional therapies, including NSAIDs and TNFa or IL-17A monoclonal antibodies, have improved symptom control but remain limited by partial efficacy, high relapse rates, and the generation of anti-drug antibodies that reduce long-term therapeutic benefits. Bimekizumab, a monoclonal antibody targeting both IL-17A and IL-17F, has shown promising clinical efficacy in AS by more comprehensively inhibiting the IL-17 axis. However, biologic agents like BKZ remain susceptible to immunogenicity-related limitations. Thus, improving delivery strategies that can enhance efficacy and reduce immunogenicity is critical.
朱露露 (Thu,) studied this question.