  Disease psoriasis occurs as chronic inflammation of skin and appears as scaly
red lesions on skin surface. Advent of several immunosuppressive drugs
established that the disease stems from immuno-pathogenic disorder in human
blood. Cell biological as well as clinical research on the disease reveals that
the helper T-cells and other Leucocytes, responsible for human immunity, may
lead to psoriasis pathogenesis if produced in plenty at locations close to the
dermal region. Research findings also showed that a complex, self-sustaining
(cytokine and related) proteins network play important role in disease
maturation by actually leading to a huge proliferation of epidermal
keratinocytes. Disease pathogenesis is identified with such hyperproliferation
leading to flaking of skin surface (psoriatic plaques). An excessive generation
of nitric oxide by proliferated keratinocytes, through a complex chain of
bio-chemical events, is causal to the scaliness of psoriatic plaques.
Considering these immunopathogenic mechanisms, we propose and analyse a
mathematical time differential model for the disease psoriasis. Outcomes of
analysis are consistent with existing cell biological and clinical findings
with some new predictions which could be tested further.
