Enzyme phosphorylation systems involving cAMP-dependent protein kinase may play a role in signal transduction and control of cell growth. TPA exerts its effects through activation of protein kinase C, which may be involved in the pathophysiology of psoriasis.
Current evidence emphasizes the role of cytokines and inflammation in the pathogenesis of psoriasis.
In the dermis, these cells release inflammatory cytokines that may stimulate the epidermal hyperproliferation in psoriasis. 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.