The skin consists of three main layers: the epidermis, dermis, and hypodermis. The epidermis is composed of keratinocytes arranged in distinct layers that serve as a physical barrier, preventing moisture loss and blocking pathogens. The dermis, below the epidermis, contains immune cells that regulate inflammation, while the hypodermis provides insulation and energy storage. Inflammation or injury activates these immune cells, triggering cytokine release to maintain barrier function and heal damage.

In psoriasis, an immune-mediated skin disorder, this barrier becomes disrupted. Hyperproliferation of keratinocytes leads to the formation of thick, scaly plaques that compromise the skin’s protective function. Immune cells, such as T-helper 17 cells, play a key role in this process by releasing pro-inflammatory cytokines like IL-17 and IL-22, which stimulate keratinocyte proliferation. Additionally, dysregulated tight junctions and abnormal lipid composition in the stratum corneum weaken the physical barrier. These changes, coupled with genetic and environmental factors, lead to chronic inflammation, making psoriasis a complex disease requiring targeted therapies that address both the physical and immune barrier disruptions.

Reference: Orsmond A, Bereza-Malcolm L, Lynch T, et al. Skin Barrier Dysregulation in Psoriasis. Int J Mol Sci. 2021 Oct 7;22(19):10841. doi: 10.3390/ijms221910841.