Activation of infiltrating T cells with cytokine release appears to be critical to the maintenance of the psoriatic lesion. Drugs such as cyclosporine, which can inhibit the synthesis of IL-2 and prevent the proliferation of T cells and their release of cytokines, are effective in the treatment of psoriasis. Similarly, dermal endothelial cells, monocytes, keratinocytes, and fibroblasts produce increased amounts of IL-6, another inflammatory cytokine, which can be inhibited by corticosteroids and calcitriol. Neuropeptides and other mediators of inflammation, such as arachidonic acid metabolites, calmodulin, and polyamines, play a role in the immunoregulation of psoriasis. Increases in the level of substance P have been detected in the nerve fibers of lesional psoriatic skin.
Several observations suggest a genetic basis for psoriasis.
One third of persons affected have a positive family history. I histocompatibility antigens associated with psoriasis. Current evidence points to genetic heterogeneity. Both autosomal dominant inheritance with incomplete penetrance and a polygenic or multifactorial inheritance may occur. A psoriasis susceptibility gene located on the distal long arm of human chromosome 17 has been identified in 65 cases of psoriasis in eight families.