Psoriasis is a prevalent chronic inflammatory skin condition characterized by relapsing and remitting flare-ups. Recent research has significantly advanced our understanding of the disease’s underlying mechanisms, revealing a complex network of interactions between immune cells and other cellular components. Central to the pathogenesis of psoriasis is a pathogenic triad involving dendritic cells, TH17 cells, and keratinocytes. Dendritic cells produce TNF-α and IL-23, which drive the differentiation of T cells into TH17 cells. These TH17 cells, in turn, secrete key cytokines such as IL-17, IFN-γ, and IL-22, leading to skin inflammation and the activation and hyperproliferation of keratinocytes. In addition to this triad, other immune cells, such as TH9 and TH22 cells, CD8+ cytotoxic T cells, neutrophils, and γδ T cells, as well as the cytokines and chemokines they release, also play significant roles in the disease’s progression. Advancements in high-throughput analysis of lesional skin have uncovered new signaling pathways and cell populations involved in psoriasis, expanding our knowledge of the immune response and disease mechanisms. These findings have revolutionized both our understanding of psoriasis pathogenesis and the clinical management of the disease.

The review aims to provide an in-depth overview of the immune dysregulation seen in psoriasis, focusing on recent discoveries. It details the involvement of various immune cells, including T cells, B cells, dendritic cells, neutrophils, monocytes, mast cells, and innate lymphoid cells (ILCs), along with non-immune cells like keratinocytes, fibroblasts, endothelial cells, and platelets, in the initiation, development, and progression of psoriasis. Understanding these immune mechanisms is vital for the development of new therapeutic approaches and improving the clinical management of psoriasis.

Reference: Sieminska I, Pieniawska M, Grzywa TM. The Immunology of Psoriasis-Current Concepts in Pathogenesis. Clin Rev Allergy Immunol. 2024 Apr;66(2):164-191. doi: 10.1007/s12016-024-08991-7. Epub 2024 Apr 20. PMID: 38642273; PMCID: PMC11193704.