Psoriasis is a chronic skin condition with a wide range of clinical manifestations, including plaque, flexural, guttate, pustular, and erythrodermic lesions. It is an immune-mediated inflammatory condition with a strong hereditary component. It may be triggered by skin damage, infection, stress, and certain medication.
Psoriasis is distinguished by epidermal proliferation and immune cell infiltration of the dermis. Psoriasis etiology is multifaceted, including the interaction of keratinocytes, immune cells, and other skin-resident cells. Activation of plasmacytoid dendritic cells (pDCs) increases the maturation and synthesis of TNF-, IL-12, and IL-23 by myeloid dendritic cells (mDCs), which leads to the activation of Th (T helper) 1 and Th17 and subsequent secretion of inflammatory cytokines such as TNF-, IL-17, IL-21, and IL-22. These cytokines subsequently activate keratinocytes, which generate antimicrobial peptides, cytokines, and chemokines, leading to the amplification of inflammation.
IL-15 is a cytokine that plays a role in innate and adaptive immunity. In addition, it acts as a growth factor and promotes the survival of T, B, and NK cells by preventing apoptosis.