The 'inflammazone' in chronic inflammatory diseases: psoriasis and sarcoidosis.

Abstract

Chronic inflammatory diseases show significant heterogeneity in their phenotypes, with diverse immune cells and mediators interacting in response to various stimuli. This review proposes the concept of the 'inflammazone' framework - which maps the distribution of immune components driving disease pathogenesis - using sarcoidosis and psoriasis as examples. Sarcoidosis features granulomatous inflammation with macrophages and CD4⁺ T cells, which can spread to lymph nodes and other organs. Psoriasis, affecting primarily the skin, involves Th1, Th17, and Th22 pathways with CD8⁺ T cells and dendritic cells. Human sarcoidosis exhibits geographic and racial variability, while psoriasis shows varying morphologies and disease courses. Sarcoidosis has more extensive distal immune signaling, whereas psoriasis remains more localized. Understanding the inflammazone is crucial for advancing personalized treatments for inflammatory diseases.