Pathophysiology of psoriasis: A review

Area of Science:

• Immunology
• Dermatology
• Genetics

Background:

• Psoriasis is a chronic inflammatory skin disease affecting ~2% of the global population.
• Its pathogenesis involves genetic factors, environmental triggers, and immune system dysregulation.
• Recent advances highlight the roles of tumor necrosis factor-α, IL-23p19, and the IL-17A axis.

Purpose of the Study:

• To review the pathophysiology of psoriasis focusing on the immune inflammatory loop.
• To discuss the roles of keratinocyte danger signals and key cytokines like IL-17 and IL-23p19.
• To explore the contribution of innate lymphoid cell 3 (ILC3) in psoriasis development.

Main Methods:

• Review of current literature on psoriasis pathogenesis.
• Analysis of immunological pathways, including T helper 17 cells and ILC3.
• Discussion of cytokine signaling and keratinocyte-derived danger signals.

Main Results:

• Innate lymphoid cell 3 (ILC3) directly induces psoriasis lesions independent of T-cell activation.
• Increased ILC3 numbers are observed in psoriatic skin and blood.
• Psoriasis is linked to comorbidities like cardiovascular disease and metabolic syndrome.

Conclusions:

• The accelerated immunological inflammatory loop, driven by cytokines like IL-23p19 and IL-17, is central to psoriasis.
• ILC3s are significant contributors to psoriasis pathogenesis.
• Further research into these pathways may lead to improved therapeutic strategies.