Potential Immunological Links Between Psoriasis and Cardiovascular Disease

Abstract

Preclinical and clinical research provide strong evidence that chronic, systemic inflammation plays a key role in development and progression of atherosclerosis. Indeed, chronic inflammatory diseases, such as psoriasis, are associated with accelerated atherosclerosis and increased risk of cardiovascular events. Contemporary research has demonstrated plausible mechanistic links between immune cell dysfunction and cardiometabolic disease in psoriasis. In this review, we describe the role of potential common immunological mechanisms underlying both psoriasis and atherogenesis. We primarily discuss innate and adaptive immune cell subsets and their contributions to psoriatic disease and cardiovascular morbidity. Emerging efforts should focus on understanding the interplay among immune cells, adipose tissue, and various biomarkers of immune dysfunction to provide direction for future targeted therapy.

Keywords: atherosclerosis; cardiovascular disease; inflammation; inflammatory cytokines; psoriasis; vascular inflammation.

Figure 1

Systemic effects of chronic low-grade inflammation in psoriasis. (A) Psoriasis, both cutaneous and arthritic, is a low-grade chronic, systemic inflammatory disease associated with increased circulating pro-inflammatory cytokines. (B) Chronic inflammation in psoriasis is associated with adipose tissue dysfunction characterized by pro-inflammatory cytokines and adipokines associated with endothelial dysfunction. (C) Furthermore, psoriasis exhibits a deranged lipid profile and impaired HDL function, which in combination with chronic inflammation accelerate atherosclerotic vascular disease. (D) The vessel wall is infiltrated through a complex interplay of pro-inflammatory cellular components, cholesterol crystals, and various lipoproteins. Over the time, with build-up of the plaque, this atherosclerotic lesion poses a significant threat to blood flow and is prone to rupture, often accelerated by inflammation leading to myocardial infarction. (E) Thus, psoriasis and psoriatic arthritis upregulate T-cell, neutrophil chemotaxis, and keratinocyte activation and endothelial dysfunction leading to increased atherosclerosis in blood vessels. Abbreviations: TNF-α, tumor necrosis factor-alpha; IL, interleukin; IFN-γ, interferon-gamma.