Psoriatic lesions are produced and maintained by alterations in cutaneous immune responses, mediated by dendritic cells activated by Toll-like receptors, producing a cascade of cytokines (TNFα, IL-17, IL-23 and IL-12), which trigger the hyperproliferation of keratinocytes in the epidermis and give rise to the appearance of epidermal hyperplasia typical of psoriasis [32]. Here, TNF is linked to psoriasis.