  Analytical research of results of experimental and theoretical studies on
pathogenesis of psoriatic disease is carried out. The new model of pathogenesis
- skin reaction to systemic psoriatic process SPP is formulated. ... Psoriatic
inflammation is regarded as a reaction of the skin immune system to activity of
Mo-R and DC-R involved in derma from blood flow. They contain Y-antigen and,
getting to derma, can be transformed in mature maDC-Y and present this antigen
to Y-specific T-lymphocytes as well as activate them. Y-antigen is a part of
the interpeptide bridge IB-Y. Therefore, the skin immune system can incorrectly
interpret Y-antigen presentation as a sign of external PsB-infection and switch
one of mechanisms of protection against bacterial infection - epidermal
hyperproliferation. Psoriatic plaque can be initiated only during action of
local inflammatory process LP2 in derma causing not only innate, but also
adaptive response. In particular, it is possible at LP2(IN) - open trauma of
derma or at LP2(HPV) - HPV-carriage of keratinocytes. The level of Y-priming
(presence and concentration of Y-specific T-lymphocytes in prepsoriatic derma
and in lymph nodes) also determines possibility of psoriatic plaque initiation.
Existence and severity of psoriatic plaque is determined by intensity of
Y-antigen income into derma (inside Mo-R and DC-R). ... Severity of plaque is
aggravated by LP2-inflammation if it persists after this plaque initiation. New
Mo-T, DC-T (incl. Mo-R, DC-R) and Y-specific T-lymphocytes are constantly
attracted into plaques from blood flow, and so support vicious cycles. Only at
decrease of SPP severity, these vicious cycles weaken and natural remission of
plaques takes place, up to their complete disappearance. The detailed analysis
comparing the new model of pathogenesis with five other previously published
models is carried out. Part 1. arXiv:1110.0584
