IFN-I Mediates Dysfunction of Endothelial Progenitor Cells in Atherosclerosis of Systemic Lupus Erythematosus.

Xuewei Ding,Xiaojie He,Wei Xiang

doi:10.3389/fimmu.2020.581385

Abstract

Systemic lupus erythematosus (SLE) is a multi-system autoimmune disease including the cardiovascular system. Atherosclerosis is the most common cardiovascular complication of SLE and a significant risk factor for morbidity and mortality. Vascular damage/protection mechanism in SLE patients is out of balance, caused by the cascade reaction among oxidative stress, proinflammatory cytokines, Neutrophil Extracellular Traps, activation of B cells and autoantibodies and abnormal T cells. As a precursor cell repairing vascular endothelium, endothelial progenitor cells (EPCs) belong to the protective mechanism and show the reduced number and impaired function in SLE. However, the pathological mechanism of EPCs dysfunction in SLE remains ill-defined. This paper reviews the latest SLE epidemiology and pathogenesis, discusses the changes in the number and function of EPCs in SLE, expounds the role of EPCs in SLE atherosclerosis, and provides new guidance and theoretical basis for exploring novel targets for SLE treatment.

Highlights

Systemic lupus erythematosus (SLE) is an immune complex-mediated autoimmune disease involving multiple systems
SLE is an autoimmune disease characterized by cardiovascular disease (CVD)
Current studies have demonstrated that the inherent factors of SLE are independent risk factors for the premature occurrence of atherosclerosis in SLE patients [4]

Summary

Introduction

SLE is an immune complex-mediated autoimmune disease involving multiple systems. Its prevalence and incidence rate can be as high as 241/100,000 per year and 23.2/100,000 per year, and the rate of premature death is 2–3 times that of healthy people [1]. IFN-a promotes endothelial dysfunction by accelerating endothelial cells (ECs) apoptosis and damaging EPCs, one of the vascular repair mechanisms [15, 46,47,48,49,50,51,52,53]. Abnormal T cell subsets are considered to be an essential factor leading to endothelial dysfunction and CVD in SLE patients.

Results

Conclusion