<unk>  is characterized by an abnormally excessive and rapid growth of the epidermal layer of the skin. Abnormal production of skin cells (especially during wound repair) and an overabundance of skin cells result from the sequence of pathological events in<unk> . The sequence of pathological events in<unk>  is thought to start with an initiation phase in which an event (skin trauma, infection, or drugs) leads to activation of the immune system and then the maintenance phase consisting of chronic progression of the disease. Skin cells are replaced every 3–5 days in<unk>  rather than the usual 28–30 days. These changes are believed to stem from the premature maturation of keratinocytes induced by an inflammatory cascade in the dermis involving dendritic cells, macrophages, and T cells (three subtypes of white blood cells). These immune cells move from the dermis to the epidermis and secrete inflammatory chemical signals (cytokines) such as interleukin-36γ, tumor necrosis factor-α, interleukin-1β, interleukin-6, and interleukin-22. These secreted inflammatory signals are believed to stimulate keratinocytes to proliferate. One hypothesis is that<unk>  involves a defect in regulatory T cells, and in the regulatory cytokine interleukin-10. The inflammatory cytokines found in<unk> oriatic nails and joints (in the case of<unk> oriatic arthritis) are similar to those of<unk> oriatic skin lesions, suggesting a common inflammatory mechanism. Gene mutations of proteins involved in the skin's ability to function as a barrier have been identified as markers of susceptibility for the development of<unk> . Deoxyribonucleic acid (DNA) released from dying cells acts as an inflammatory stimulus in<unk>  and stimulates the receptors on certain dendritic cells, which in turn produce the cytokine interferon-α. In response to these chemical messages from dendritic cells and T cells, keratinocytes also secrete cytokines such as interleukin-1, interleukin-6, and tumor necrosis factor-α, which signal downstream inflammatory cells to arrive and stimulate additional inflammation. Dendritic cells bridge the innate immune system and adaptive immune system. They are increased in<unk> oriatic lesions and induce the proliferation of T cells and type 1 helper T cells (Th1). Targeted immunotherapy, as well as<unk> oralen and ultraviolet A (PUVA) therapy, can reduce the number of dendritic cells and favors a Th2 cell cytokine secretion pattern over a Th1/Th17 cell cytokine profile.<unk> oriatic T cells move from the dermis into the epidermis and secrete interferon-γ and interleukin-17. Interleukin-23 is known to induce the production of interleukin-17 and interleukin-22. Interleukin-22 works in combination with interleukin-17 to induce keratinocytes to secrete neutrophil-attracting cytokines.
Psoriasis
Onychomycosis
Parapsoriasis
Basal-cell carcinoma
Lupus vulgaris
Dermatitis
Vitiligo
Dandruff