NETs in APS: Current Knowledge and Future Perspectives
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ANTIPHOSPHOLIPID SYNDROME (S ZUILY, SECTION EDITOR)
NETs in APS: Current Knowledge and Future Perspectives Ajay Tambralli 1,2 & Kelsey Gockman 2 & Jason S. Knight 2
# Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Purpose of Review Antiphospholipid syndrome (APS) is a thrombo-inflammatory disease that is primarily treated with anticoagulation. Better understanding the inflammatory aspects of APS could lead to safer, more effective, and more personalized therapeutic options. To this end, we sought to understand recent literature related to the role of neutrophils and, in particular, neutrophil extracellular traps (NETs) in APS. Recent Findings Expression of genes associated with type I interferons, endothelial adhesion, and pregnancy regulation are increased in APS neutrophils. APS neutrophils have a reduced threshold for NET release, which likely potentiates thrombotic events and perhaps especially large-vein thrombosis. Neutrophil-derived reactive oxygen species also appear to play a role in APS pathogenesis. There are new approaches for preventing and disrupting NETs that could potentially be leveraged to reduce the risk of APS-associated thrombosis. Summary Neutrophils and NETs contribute to APS pathophysiology. More precisely understanding their roles at a mechanistic level should help identify new therapeutic targets for inhibiting NET formation, enhancing NET dissolution, and altering neutrophil adhesion. Such approaches may ultimately lead to better clinical management of APS patients and thereby reduce the chronic burden of this disease. Keywords Antiphospholipid syndrome . Neutrophils . Neutrophil extracellular traps . Interferons . Reactive oxygen species
Introduction Antiphospholipid syndrome (APS) is an acquired autoimmune thrombo-inflammatory disease characterized by vascular thrombosis and pregnancy morbidity in the presence of one or more antiphospholipid antibodies (aPL). The aPL that fulfill current classification criteria include the lupus anticoagulant (actually a functional assay that denotes the presence of potentially diverse aPL in a plasma sample), anti-cardiolipin antibodies (aCL), and anti-beta-2 glycoprotein I antibodies (aβ2GPI) [1, 2]. Beyond thrombosis and pregnancy loss, This article is part of the Topical Collection on Antiphospholipid Syndrome * Jason S. Knight [email protected] 1
Division of Pediatric Rheumatology, Department of Pediatrics, University of Michigan, Ann Arbor, MI, USA
2
Division of Rheumatology, Department of Internal Medicine, University of Michigan, 1150 West Medical Center Drive, Ann Arbor, MI 48109-5678, USA
APS is also associated with a spectrum of extra criteria manifestations, including valvular heart disease, neurologic manifestations (cognitive dysfunction, chorea, seizures), nephropathy, livedo reticularis, pulmonary hypertension, and thrombocytopenia, among others [2, 3]. The prevalence of primary APS is thought to be as high as 0.05% of the population, with additional cases detected as a secondary manifestation of ano
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