• Unraveling the Immune Web of Psoriasis: From Inflammatory Memory to Targeted Therapies
  • Ali Bejani,1 Majid Sadeghpour,2 Nasrin Moghimi,3,*
    1. Student Research Committee, Kurdistan University of Medical Sciences, Sanandaj, Iran
    2. Department of General Medicine, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
    3. Cancer & Immunology Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran.


  • Introduction: Psoriasis is a chronic, inflammatory skin disease characterized by dysregulated immune responses and systemic inflammation. Affecting 1-3% of the global population, its etiology remains incompletely understood, with contributions from genetic, environmental, and immune factors. The past few decades have seen significant advancements in understanding its pathophysiology, highlighting the roles of immune cells, keratinocytes, and cytokines. This review aims to present recent findings in psoriasis research, focusing on immune mechanisms and emerging therapeutic strategies.
  • Methods: A comprehensive literature search was conducted using PubMed, Scopus, and Web of Science databases. Studies were selected based on relevance to the pathophysiology, immune involvement, and treatment outcomes of psoriasis. Key terms included "psoriasis," "immune response," "biologic therapy," "inflammatory memory," and "T cells."
  • Results: Recent studies have revealed crucial insights into the immune mechanisms underlying psoriasis. The routine use of targeted immunomodulatory therapies has transformed patient outcomes, with skin clearance rates of up to 60% at one year. However, recurrence often follows drug withdrawal due to the persistence of inflammatory memory in the skin, primarily driven by tissue-resident memory T cells, Langerhans cells, and dermal dendritic cells. Additionally, γδ T cells, known for producing IL-17, have been identified as key mediators of repeated psoriatic inflammation, exhibiting memory-like characteristics in epithelial tissues. These cells are implicated in both host defense and immune dysregulation, reinforcing their importance in psoriasis and other inflammatory conditions. The immune landscape of psoriasis involves multiple cell types, including TH17, dendritic cells, and keratinocytes, which create a pathogenic triad. Emerging evidence from high-throughput studies has expanded our understanding of signaling pathways and cell populations, including TH9, TH22, and γδ T cells. These discoveries have revolutionized the clinical management of psoriasis, paving the way for personalized treatment approaches that aim to sustain remission while reducing long-term drug burdens. Research into B cells also suggests a potential role in exacerbating psoriasis, particularly through autoantibody production and pro-inflammatory cytokine release.
  • Conclusion: The pathogenesis of psoriasis is a complex interplay of immune cells and cytokines, which not only drives skin inflammation but also contributes to systemic effects, such as psoriatic arthritis. Targeted therapies, including biologics, have significantly improved patient outcomes, but challenges remain in maintaining long-term remission. Understanding the immune mechanisms, including the roles of T cells, dendritic cells, and emerging players like B cells, is essential for developing more effective and sustainable treatments. Future research should continue exploring immune dysregulation in psoriasis, with the goal of reducing the reliance on long-term therapies while preventing recurrence
  • Keywords: Psoriasis, Immune dysregulation, Inflammatory memory, Biologic therapy, T cells