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Psoriasis presents one of the numerous disorders, connected with the unbalance of the system of Th1-Cytokines and Th2 -Cytokines. The activation of Th1CD4 + lymphocytes is a result of their instruction by the antigen-representing cells of the body itself in response to the antigen, whose nature is thus far unknown.
According to one of the theories that support the infectious theory of psoriasis, there is an overlapping of the epitopes of an antigen of one of the representatives of staphylococci with the surface protein of M keratinocytes of a human (so-called cross-presentation phenomenon). There is formed a pool of Cytotoxic Lymphocytes (CTL) which attacks the keratinocytes of the skin of a human, causing their premature Apoptosis (programmed cell death). And if normal keratinocytes live for 27-30 days, the time of their life in the people with psoriasis is no more than 9 days. As a result there are formed an accumulations of the dead cells, not connected with the bare inflammatory surface of the skin, in which there develops a classical autoimmune reaction.
Local inflammation with the activation of Th1-cytokines (IL-1, IL-2, TNF-A), chemokines (IL-8), activators of transcription (Nuclear factor kB (Nuclear factor-kappa B; NF-kB)), metal proteinases, which all together stimulate Angiogenesis (process involving the growth of new blood vessels from pre-existing vessels) with the increase in the Vessel Endothelium (VEGF), all this forms the combination of the classical signs of psoriasis, which morphologically acquires the form of so-called "psoriatic plaque" with the triad of the signs: peeling, elevation above the skin, blood supply.
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