A Cellular Automaton Model for Psoriasis Disease

摘要

Psoriasis is a highly prevalent autoimmune disorder of the skin, which manifests clinically via the formation of a thickened epidermis, and a scale-like appearance in affected regions known as psoriatic plaques. The disease is highly complex, arising at least in part via a systemic perturbation of cytokine and chemokine dynamics. In addition, psoriasis is both genetically and phenotypically heterogeneous, with patients displaying highly diverse molecular profiles and plaque structures. An understanding of the differences driving phenotypic diversity in psoriasis, and other complex diseases, is thus essential to positing more effective and personalised therapeutics. In this paper we develop and implement a cellular automaton model, based on the biology of psoriasis plaque formation as one case study, to investigate the mechanisms of psoriasis (and other complex disease) heterogeneity. Our preliminary model is capable of simulating a wide array of clinically relevant plaque structures, for given parameter regimes, in a manner that permits hypotheses to be generated and tested, on the molecular mechanisms driving the differences between the different clinical phenotypes. The proposed modelling approach is general enough to be applied to other complex diseases.