Inflammatory niches as spatial drivers of disease mechanisms and targets for personalized treatment

Disease states are increasingly recognized as being shaped by spatially organized inflammatory niches, in which immune and non-immune cells coordinate diverse biological processes, including tissue development, homeostasis and pathology. The activation and composition of specific inflammatory responses, as well as the signalling pathways involved, are highly context- and location-dependent. Recent technological advances-particularly the integration of single-cell sequencing with spatial profiling-have greatly enhanced our ability to dissect these processes at a molecular level. Such approaches have revealed disease-specific mechanisms, including IL-36-driven feed-forward amplification in the upper layers of psoriatic epidermis, the complex inflammatory architecture of hidradenitis suppurativa and T-cell-basal keratinocyte interactions in lichen planus. Continued investigation of inflammatory niches across diseases will deepen our understanding of their pathogenic mechanisms, enable the identification of patient-specific cellular networks and pave the way for more personalized therapeutic strategies.