From rheumatology to dermatology: cytokine signaling pathways as therapeutic targets at the skin–joint interface in inflammatory diseases: a narrative review

Over the last two years, inflammatory dermatology has undergone a transition from morphology-based classification toward pathway-driven immune endotyping. Atopic dermatitis, psoriatic disease, and hidradenitis suppurativa have emerged as paradigmatic models of this transition, illustrating how epithelial dysfunction, involving autoinflammation and adaptive immunity, may lead to systemic inflammatory crosstalks, connecting cutaneous and musculoskeletal manifestations. Recent studies have refined the understanding of progressive immune maturation in atopic dermatitis, while psoriasis and juvenile psoriatic arthritis support skin-to-joint inflammatory models involving IL-23/IL-17 signaling. Hidradenitis suppurativa is increasingly recognized as a systemic autoinflammatory disease within a broader neutrophilic inflammatory spectrum. Parallel therapeutic advances involving IL-17, IL-23, TNF, and JAK inhibition reinforced the translational importance of these discoveries and accelerated the development of precision dermatology strategies.