Potential Immunological Links Between Psoriasis and Cardiovascular Disease.

Aparna P Sajja,Nehal N Mehta,Aditya A Joshi,Amit K Dey,Heather L Teague

doi:10.3389/fimmu.2018.01234

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.

Highlights

Inflammation is the hallmark of atherosclerosis [1]
Novel evidence has recently suggested that a complex interplay involving neutrophil–macrophage cross-talk is crucial to the process of atherosclerosis and acute coronary syndrome (ACS) [106,107,108]. As these cells are involved throughout the process of atherosclerosis from plaque development to complications, such as ACS, and play a significant role in psoriasis, further research may provide new avenues for treatment of both these conditions
neutrophil extracellular traps (NETs) may be involved in the initial injury of the endothelium during atherogenesis, with recent evidence demonstrating the presence of neutrophils and NETs at sites of plaque rupture and endothelial cell erosion in human carotid plaques, features which we hypothesized would be evident in early atherosclerosis in psoriasis

Summary

Introduction

Inflammation is the hallmark of atherosclerosis [1]. Preclinical and clinical research provide strong evidence that chronic inflammation is critical to the process of atherogenesis. In order to speed understanding of inflammatory cardiometabolic dysfunction, psoriasis has been utilized as a human model [3] to understand the role of innate and adaptive immunity in subclinical CVD [43, 44]. Th1 subtype is the most studied cell-type in psoriasis, different stages of this chronic inflammatory disease employ various cells of innate and adaptive immunity [62].

Results

Conclusion