Inflammatory immune mechanisms underlying the comorbidity of psoriasis and atherosclerosis: clinical implications

Psoriasis (PSO) is a chronic immune-mediated inflammatory disease and an independent risk factor for cardiovascular disease (CVD), particularly atherosclerosis (AS). Both disorders share common immunopathological pathways characterized by persistent systemic inflammation and dysregulated interactions between innate and adaptive immunity.

In this review, we summarize the shared immunoinflammatory mechanisms linking psoriasis and atherosclerosis and highlight potential therapeutic strategies targeting cutaneous manifestations and systemic comorbidities.

Dendritic cells (DCs), macrophages, neutrophils, and T lymphocytes contribute to a proinflammatory milieu that affects not only the skin but also the vasculature. The interleukin-23 (IL-23)/T helper 17 (Th17) axis plays a central role in inducing proinflammatory cytokines such as interleukin-17 (IL-17), tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β), thereby promoting endothelial dysfunction, oxidative stress, and vascular inflammation. In turn, activation of pattern-recognition receptors and the NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome amplifies inflammatory responses, linking keratinocyte (KC) hyperproliferation to vascular injury. Collectively, these processes may form a self-perpetuating inflammatory network that links cutaneous inflammation to CVD.

In this review, we provide a comprehensive overview of the immunological interactions underlying the psoriasis-atherosclerosis connection and highlight potential therapeutic strategies targeting both cutaneous manifestations and systemic comorbidities.