Psoriasis and Cardiovascular Diseases: An Immune-Mediated Cross Talk?

Abstract

Psoriasis is a chronic immune-mediated inflammatory skin disease, characterized by well-demarcated scaly, erythematous, infiltrated plaques. The cutaneous-to-systemic expansion of the inflammation in psoriasis leads to the concept of "psoriatic march" or "inflammatory skin march". Accordingly, psoriasis is thought to be a systemic inflammatory disease associated with numerous comorbidities. Indeed, it's currently considered an independent risk factor for cardiovascular diseases. Here, we discuss the current knowledge on TNF-α and IL-23/IL-17 mediated pathways linking the psoriatic plaque to the cardiovascular compartment. We further argue the possible involvement of the endothelial compartment in the psoriatic plaque- cardiovascular system crosstalk.

Keywords: cardiovascular diseases; cytokines; endothelial dysfunction (ED); inflammation; psoriasis.

Figure 1

The immune-mediated pathogenetic link between psoriasis and cardiovascular disorders: triggering the endothelial dysfunction. In the psoriatic plaque, immune cells, including Th17 promote the generation and release of circulating inflammatory mediators as IL-17 and TNF-α. TNF-α caused NF-κB activation, subsequently leading to increased expression of multiple pro-inflammatory cytokines in the psoriatic skin. In endothelial cells, IL-17A receptor drives the production of TNF-α, IL-1β, CCL2, and the expression of ICAM- 1 leading to the endothelial dysfunction involved in the pathophysiology of multiple immune-mediated CVDs. The IL-17 also triggers the accumulation of ROS, in particular $O_2^{-}$ within the endothelium further contributing to endothelial dysfunction and CVD progression.