BSCR pathogenesis involves a Th17-mediated inflammatory response, with CD8+ and NK cell involvement. While anti-TNF agents remain an established treatment for refractory BSCR, the clinical failure of IL-17A inhibitors suggests that broader inhibition, such as dual IL-17A/F blockade, may be needed. Future studies integrating single-cell techniques and tissue-specific insights are needed to understand disease mechanism and guide treatment.
Gao et al. (Thu,) studied this question.