Dynamic Boolean modeling of molecular and cellular interactions in psoriasis predicts drug target candidates.

ABSTRACT: Psoriasis arises from complex interactions between keratinocytes and immune cells, leading to uncontrolled inflammation, immune hyperactivation, and a perturbed keratinocyte life cycle. Despite the availability of drugs for psoriasis management, the disease remains incurable. Treatment response variability calls for new tools and approaches to comprehend the mechanisms underlying disease development. We present a Boolean multiscale population model that captures the dynamics of cell-specific phenotypes in psoriasis, integrating discrete logical formalism and population dynamics simulations. Through simulations and network analysis, the model predictions suggest that targeting neutrophil activation in conjunction with inhibition of either prostaglandin E2 (PGE2) or STAT3 shows promise compa

SUBMITTER: Tsirvouli E 

PROVIDER: S-EPMC10831929 | biostudies-literature | 2024 Feb

REPOSITORIES: biostudies-literature