Endothelial progenitor dysfunction associates with a type I interferon signature in primary antiphospholipid syndrome.

ABSTRACT:

Objectives

Patients with antiphospholipid syndrome (APS) are at risk for subclinical endothelial injury, as well as accelerated atherosclerosis. In the related disease systemic lupus erythematosus, there is a well-established defect in circulating endothelial progenitors, which leads to an accrual of endothelial damage over time. This defect has been at least partially attributed to exaggerated expression of type I interferons (IFNs). We sought to determine whether these pathways are important in APS.

Methods

We studied 68 patients with primary APS. Endothelial progenitors were assessed by flow cytometry and functional assay. Type I IFN activity was determined by a well-accepted bioassay, while peripheral blood mononuclear cells were scored for expression of IFN-responsive g

SUBMITTER: Grenn RC 

PROVIDER: S-EPMC5233467 | biostudies-literature | 2017 Feb

REPOSITORIES: biostudies-literature