<unk>  is an immune-mediated disease with a genetic predisposition, though no specific immunogen has been implicated in the development of<unk> . The pathophysiology of<unk>  consists of interactions between cytokines, dendritic cells, and T lymphocytes (particularly Th1 and Th17). Common triggers of<unk>  include injury to the skin, trauma, infection, and medications. T cells play a key role in the pathogenesis of<unk>  via the production of pro-inflammatory cytokines. Certain genes increase the likelihood of developing<unk> ; the first gene that was discovered to be linked to the development of<unk>  was HLA-Cw6, which is located at PSORS1 at chromosomal position 6p21.3. Microscopically, skin affected by<unk>  displays parakeratosis, acanthosis, hyperkeratosis, Kogoj pustules, and Munro's microabscesses. The red appearance of psoriatic lesions is due to dilated blood vessels in the skin.
Psoriasis pathophysiology
Eczema pathophysiology
Vitiligo pathophysiology
Dermatophytosis pathophysiology
Squamous cell carcinoma of the skin pathophysiology
Herpes simplex pathophysiology
Scleroderma pathophysiology
Skin cancer pathophysiology