ReviewFrontiers in immunology2026
The role of neutrophil extracellular traps in antiphospholipid syndrome.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
Antiphospholipid syndrome (APS) is an acquired systemic autoimmune disorder characterized clinically by recurrent arterial and venous thrombosis and/or adverse pregnancy outcomes, and laboratory-defined by persistently positive antiphospholipid antibodies (aPLs). Neutrophils are the most abundant white blood cells in the circulation. In APS patients, aPLs abnormally activate neutrophils, causing them to transition from a quiescent state to a highly activated state, which is a central mechanism in disease pathogenesis. Neutrophil extracellular traps (NETs) are reticular structures composed of DNA, histones, and granular proteins released by neutrophils under stress conditions. As a crucial immune mechanism for neutrophil function, NETs play a vital role in anti-infection and immune responses. However, when overactivated or lacking inhibition, NETs can mediate the development of various diseases. Recent studies indicate that neutrophils and NETs occupy a central position in APS pathogenesis, promoting thrombosis and contributing to pathological processes such as placental dysfunction. This review summarizes the role of NETs in the development and progression of APS.
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