Modelling the pathogenesis and treatment of psoriasis

Psoriasis is a common chronic skin disorder characterised by thickening and itching of the epidermis. The pathogenesis is complex, involving a mixture of an autoimmune components, environmental cause and genetic susceptibility. Treatments include the suppression of inflammatory signalling and UV radiation.

I will describe investigations of a computational model of psoriasis, based on ordinary differential equations, predicated on the idea that skin cells exist in two lineages, psoriatic and normal, that compete with one another. The psoriatic cells have greater proliferation rates but can be suppressed by normal cells. I show how the model can simulate the development of psoriasis and its resolution by a UV-treatment protocol, and show fitting results intended to improve the model's concordance with experiment. This model is compared with a simpler ODE model of a single lineage responding to growth signals, and also with an agent-based model previously developed here in Newcastle.

I also put this project in the context of the PSORT project which brings together several academic and industry partners.