Open AccessNetosis in the pathogenesis of antiphospholipid syndrome and systemic lupus erythematosus
Author(s) -
К. С. Нурбаева,
Т. М. Решетняк,
А. М. Лила
Publication year - 2021
Publication title -
sovremennaâ revmatologiâ
Language(s) - English
Resource type - Journals
eISSN - 2310-158X
pISSN - 1996-7012
DOI - 10.14412/1996-7012-2021-5-96-102
Subject(s) - neutrophil extracellular traps , pathogenesis , antiphospholipid syndrome , immunology , medicine , autoimmune disease , inflammation , extracellular , thrombosis , disease , lupus erythematosus , systemic lupus erythematosus , autoimmunity , systemic disease , antibody , immunopathology , biology , pathology , microbiology and biotechnology
Antiphospholipid syndrome (APS) and systemic lupus erythematosus (SLE) are autoimmune diseases. In recent years, APS has been considered as an autoimmune thrombo-inflammatory disease. It has been established that clinical manifestations of APS can persist, progress over time, or debut during an adequate anticoagulant therapy and, in some cases, require administration of immunosuppressive drugs, which indicates the role of autoimmune inflammation in their development. The formation of extracellular neutrophil traps (neutrophil extracellular traps, NETs) is one of the connecting links of inflammation and thrombosis. Netosis is the process by which activated neutrophils in the extracellular space form netlike structures (NETs). This review examines the role of neutrophils and netosis in the pathogenesis of APS and SLE.