Psoriasis Awareness Month

Psoriasis is a chronic, currently non-curable, immune-mediated skin disorder marked by inflamed, scaly patches that commonly affects the elbows, knees, scalp, and trunk [1]. The scaly patches can be itchy, causing soreness and potentially leading to disfiguration [2]. Globally, psoriasis affects approximately 1–3% of the population, amounting to over 100 million cases worldwide [3]. In the UK, recent estimates indicate about 1.1 million people — roughly 1.7% to 2.8% of the population — are affected by psoriasis[4]. The significant prevalence of psoriasis, combined with its impact on quality of life, drives the market growth of related drug research. In 2025, the market is estimated at $20.9B with a growth of 6.9% in the next 7 years [5].

Cellomatics has established robust in vitro platforms for evaluating novel therapeutics in psoriasis, leveraging expertise in immunology, inflammation and complex skin biology. Our models include primary human keratinocytes or immortalised keratinocyte lines, used as monocultures or in co-culture with freshly isolated peripheral blood mononuclear cells (PBMCs) to capture immune–epithelial interactions. To enhance physiological relevance, three-dimensional skin models, such as reconstructed human epidermis (RHE), have been developed to more closely mimic the architecture and function of native skin. These systems allow the study of key features of psoriatic pathology, including keratinocyte hyperproliferation, cytokine-driven inflammation, and barrier dysfunction, providing a translational platform for drug screening and mechanistic research.

Differentiation of primary human keratinocytes was assessed under three conditions: untreated controls, calcium and serum supplementation, and exposure to a psoriasis-specific cytokine cocktail. Calcium and serum treatment promoted terminal differentiation, reflected by stratification of the keratinocyte layers. In contrast, keratinocytes exposed to the psoriasis-specific cocktail showed delayed and aberrant differentiation by Day 6 (Figure 1A), consistent with the impaired epidermal maturation characteristic of psoriasis. Furthermore, co-cultures of keratinocytes and PBMCs treated with the same cytokine cocktail elicited a strong inflammatory response (Figure 1B), demonstrating that these platforms effectively capture both defective keratinocyte differentiation and heightened immune activation, key hallmarks of psoriasis.