T cell-centric immunopathogenesis of psoriasis

Psoriasis is a chronic, immune-mediated inflammatory skin disease characterized by hyperproliferation of keratinocytes and immune cell infiltration.T cells play a central role in the immunopathogenesis of psoriasis by orchestrating a complex cytokine network that drives inflammation and epidermal alterations.Among T cell subsets, Th17 cells are particularly pivotal, producing interleukin (IL)-17A, IL-17F, and IL-22, which contribute directly to the development and maintenance of psoriatic plaques.Pathogenic Th17 cells, characterized by the production of IL-17 and other pro-inflammatory cytokines, drive chronic inflammation in psoriasis, whereas non-pathogenic Th17 cells, although also producing IL-17, contribute to tissue homeostasis and microbial defense.Importantly, IL-23 inhibitors selectively target pathogenic Th17 cells, minimizing unwanted immunosuppressive effects.Regulatory T cells (Tregs) exhibit functional impairment in psoriasis, disturbing immune tolerance and promoting pathogenic inflammation.Additionally, cutaneous tissue-resident memory T cells (TRM), marked by CD69 and CD103 expression, have been implicated in disease persistence and recurrence.T cell plasticity further complicates disease progression by allowing phenotypic switching between Th17 and Treg lineages.Understanding these immune mechanisms is critical for developing future therapeutic strategies targeting T cell-mediated pathways.