Psoriasis and psoriatic arthritis (PsA) are common diseases associated with considerable morbidity and disability. Their pathophysiology comprises a dysfunctional stromal-immune cell and cytokine network leading to inflammation of skin, entheses and joints. Recent advances in understanding of disease pathogenesis have led to the introduction of novel therapeutics providing the ultimate proof of concept in defining the role of these targets in the pathogenetic response. The pro-inflammatory cytokines TNF, IL-12/IL-23 and a variety of co-stimulator molecules have all been identified as critical factors in disease progression. In this short review we summarise key recent developments in understanding of the role of cytokines, T cells, B cells in psoriatic disease pathogenesis. We also describe the pathways that are believed to link such inflammatory pathways to articular matrix dysregulation.