  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.

Tissues and Organs;Populations and Evolution