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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.
Jiang et al. (Fri,) studied this question.