Shared inflammatory architecture and therapeutic tensions between psoriasis and Crohn's disease

Psoriasis and Crohn's disease are chronic immune-mediated inflammatory diseases affecting distinct barrier organs, yet epidemiological, genetic, transcriptomic, and therapeutic evidence supports partial immune convergence between them. This review argues that the relationship between psoriasis and Crohn's disease reflects partial immune convergence shaped by tissue context, rather than a single shared disease entity. TNF-α and IL-23-centered type 17 immunity represent the most clinically relevant shared upstream programs, whereas downstream effector pathways, especially IL-17-related responses, are shaped differently by skin and gut barrier architecture, resident immune ecology, microbial exposure, and repair demands. We discuss the gut-skin axis with caution: barrier dysfunction, dysbiosis, microbial metabolites, and immune-cell trafficking may connect skin and intestinal inflammation, but direct causal evidence in humans remains limited. TNF inhibitors, IL-12/23 blockade, and selective IL-23 inhibitors are the most plausible options for selected patients requiring treatment compatible with both skin and gut disease, whereas IL-17 blockade and paradoxical psoriasiform reactions illustrate organ-specific therapeutic tensions. Future progress will depend on patient stratification using clinical phenotypes, biomarkers, tissue profiling, and treatment history to identify patients in whom skin and intestinal inflammation are driven by overlapping immune mechanisms.